How to erase a memory — and restore it

 
Researchers at the University of California, San Diego School of Medicine have erased and reactivated memories in rats, profoundly altering the animals’ reaction to past events.

 

The study, published in the June 1 advanced online issue of the journal Nature, is the first to show the ability to selectively remove a memory and predictably reactivate it by stimulating nerves in the brain at frequencies that are known to weaken and strengthen the connections between nerve cells, called synapses.

 

“We can form a memory, erase that memory and we can reactivate it, at will, by applying a stimulus that selectively strengthens or weakens synaptic connections,” said Roberto Malinow, MD, PhD, professor of neurosciences and senior author of the study. Continue reading “How to erase a memory — and restore it”

Can Certain Herbs Stave Off Alzheimer’s Disease?

 

 

ST. LOUIS — Enhanced extracts made from special antioxidants in spearmint and rosemary improve learning and memory, a study in an animal model at Saint Louis University found.

“We found that these proprietary compounds reduce deficits caused by mild cognitive impairment, which can be a precursor to Alzheimer’s disease,” said Susan Farr, Ph.D., research professor geriatrics at Saint Louis University School of Medicine.

Farr added, “This probably means eating spearmint and rosemary is good for you. However, our experiments were in an animal model and I don’t know how much — or if any amount — of these herbs people would have to consume for learning and memory to improve. In other words, I’m not suggesting that people chew more gum at this point.”

Farr presented the early findings at Neuroscience 2013, a meeting of 32,000 on Monday, Nov. 11. She tested a novel antioxidant-based ingredient made from spearmint extract and two different doses of a similar antioxidant made from rosemary extract on mice that have age-related cognitive decline.

She found that the higher dose rosemary extract compound was the most powerful in improving memory and learning in three tested behaviors. The lower dose rosemary extract improved memory in two of the behavioral tests, as did the compound made from spearmint extract.

Further, there were signs of reduced oxidative stress, which is considered a hallmark of age-related decline, in the part of the brain that controls learning and memory.

“Our research suggests these extracts made from herbs might have beneficial effects on altering the course of age-associated cognitive decline,” Farr said. “It’s worth additional study.”

The research, which was supported by the VA Medical Center in St. Louis, was conducted in conjunction with Kemin Industries, which manufactures specialty ingredients for vitamin/dietary supplements or that can be added to food to enhance its nutritional and health benefits.

Established in 1836, the School of Medicine has the distinction of awarding the first medical degree west of the Mississippi River. The school educates physicians and biomedical scientists, conducts medical research, and provides health care on a local, national and international level. Research at the school seeks new cures and treatments in five key areas: infectious disease, liver disease, aging and brain disease, cancer and heart/lung disease.

Good hygiene may be to blame for soaring Alzheimer’s

Modern cities and improved hygiene could be behind rising rates of Alzheimer’s in Britain and the rest of the developed world, scientists have said.

Countries where everyone has access to cleaning drinking water, such as the UK and France, have nine per cent higher Alzheimer's rates then average.

Countries where everyone has access to cleaning drinking water, such as the UK and France, have nine per cent higher Alzheimer’s rates then average.  Photo: PHANIE/ALAMY

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By Laura Donnelly and agencies

4:00PM BST 04 Sep 2013

 

Researchers have linked the “hygiene hypothesis” – the idea that lack of exposure to germs, viruses and parasites harms the immune system – to rising rates of dementia in richer nations.

A new study by Cambridge University compared dementia cases in 192 countries and found it was more common in those with better sanitation and less disease.

Countries where everyone has access to cleaning drinking water, such as the UK and France, have nine per cent higher Alzheimer’s rates then average.

In comparison those where less than half have access, such as Kenya and Cambodia, have a significantly lower incident rate.

Taken together, infection levels, sanitation and urbanisation account for 43 per cent of the variation in rates of Alzheimer’s between different countries, the study found.

Dr Molly Fox, from Cambridge University, who led the new research published in the journal Evolution, Medicine and Public Health, said: “The ‘hygiene hypothesis’, which suggests a relationship between cleaner environments and a higher risk of certain allergies and autoimmune diseases, is well established.

“We believe we can now add Alzheimer’s to this list of diseases. There are important implications for forecasting future global disease burden, especially in developing countries as they increase in sanitation.”

The charity The Alzheimer’s Society said the theory was interesting, but did not demonstrate the cause of the variation.

Dr James Pickett, head of research, said: ‘We have known for some time that the numbers of people with Alzheimer’s varies between countries. That this discrepancy could be the result of better hygiene is certainly an interesting theory and loosely ties in with the links we know exist between inflammation and the disease. However it is always difficult to pin causality to one factor and this study does not cancel out the role of the many other lifestyle differences such as diet, education and wider health which we know can also have a role to play.”

Experts said that although the study allowed for the fact that people live far longer in Western countries, it did not take account of the fact that such countries had better reporting systems and were more likely to document cases of Alzheimer’s disease.

In the Cambridge study, scientists looked at the link between hygiene and Alzheimer’s rates in 192 rich and poor countries. They adjusted the findings to take account of differences in birth rate, life expectancy and age structure.

Access to clean drinking water was one area said to have a high impact on Alzheimer’s rates. Countries such as the UK and France, where this is universal, had a 9 per cent higher incidence of Alzheimer’s than countries such as Kenya and Cambodia where less than half the population can access clean water.

A similar pattern emerged from comparisons between countries with low and high rates of infectious disease.

Switzerland and Iceland, with very low rates, were 12 per cent more affected by Alzheimer’s than China and Ghana, whose infection rates are high.

The more urbanised countries also experienced higher rates of Alzheimer’s irrespective of life expectancy.

In the UK and Australia, where more than three quarters of the population lived in urban areas, Alzheimer’s incidence was 10% higher than in Bangladesh and Nepal, where less than a 10th of people had their homes in towns and cities.

Previous research has shown that Alzheimer’s affects fewer people in Latin America, China and India than it does in Europe.

Even within those regions, prevalence is lower in urban than in rural areas, according to the new findings.

The hygiene hypothesis is based on the assumption that lack of contact with “dirt” in the form of bacteria and other infectious agents upsets the development of white blood cells, key elements of the immune system.

In particular, T-cells are said to be affected. T-cells have a variety of functions, including attacking and destroying foreign invaders and marshalling other parts of the immune system.

Some, known as “regulatory” T-cells, reign in the immune system when it starts to get out of control. Dysfunctional regulatory T-cells can lead to inflammation and autoimmune disorders.

Regulatory T-cell deficiency is linked to the type of inflammation commonly found in the brains of people with Alzheimer’s disease.

The researchers wrote: “Exposure to micro-organisms is critical for the regulation of the immune system.”

Since the turn of the 19th century, such exposure had increasingly diminished in wealthier nations due to lack of contact with “animals, faeces and soil”.

“The increase in adult life expectancy and Alzheimer’s prevalence in developing countries is perhaps one of the greatest challenges of our time,” said Dr Fox.

“Today, more than 50 per cent of people with Alzheimer’s live in the developing world, and by 2025 it is expected that this figure will rise to more than 70 per cent.

“A better understanding of how environmental sanitation influences Alzheimer’s risk could open up avenues for both lifestyle and pharmaceutical strategies to limit Alzheimer’s prevalence.”

The hygiene hypothesis is normally thought to be most relevant in childhood, when the immune system is still developing. But in the case of Alzheimer’s, exposure to microbes across a person’s lifetime might be important, say the scientists. This is because regulatory T-cell numbers peak at various points in life, for example at adolescence and middle age.

161st Health Research Report 10 AUG 2013 – Synopsis

www.healthresearchreport.me 

 

 

In this issue:

1.       Plant-Based Compound May Inhibit HIV Infection, Research Shows

2.       Methamphetamine increases susceptibility to deadly fungal infection

3.       Exercise May be the Best Medicine for Alzheimer’s

4.       Study finds evidence of nerve damage in around half of fibromyalgia patients

5.       Blocking sugar intake may reduce cancer risk or progression in obese and diabetic people

6.       Fatty acids could aid cancer prevention and treatment

7.       Illinois scientists put cancer-fighting power back into frozen broccoli

8.       Diets of Pregnant Women Contain Harmful, Hidden Toxins

9.       L-3-n-butylphthalide protects against cognitive dysfunction in vascular dementia

 ScreenHunter_42 Dec. 31 12.07

Health Research Report

161st Issue Date 10 AUG 2013

Compiled By Ralph Turchiano

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Necrostatin-1 counteracts aluminum’s neurotoxic effects

 Contact: Daphne Watrin d.watrin@iospress.nl 31-206-883-355 IOS Press

 

New studies in mice support toxic role of aluminum in neurodegenerative conditions, according to report in Restorative Neurology and Neuroscience

Amsterdam, NL, August 2, 2013 – Investigators have linked aluminum accumulation in the brain as a possible contributing factor to neurodegenerative disorders such as Alzheimer’s disease. A new study published in Restorative Neurology and Neuroscience sheds light on the mechanism underlying aluminum-induced neuronal cell death and identifies necrostatin-1 as a substance which counteracts several of aluminum’s neurotoxic effects.

Researchers have long focused on why neurons die in degenerative diseases. One process is apoptosis, a form of gene-directed programmed cell death which removes unnecessary, aged, or damaged cells. When neurons die as a result of stroke, trauma, or other insult, the process is known as necrosis. Recently, a new type of necrosis, necroptosis (programmed necrosis), has been implicated in the cell demise process. In this report, the results of several experiments support the hypothesis that aluminum-induced neuronal cell death is, to a large extent, due to necroptosis, says lead investigator Qinli Zhang, PhD, of the Department of Occupational Health, Ministry of Education Key Laboratory, School of Public Health of Shanxi Medical University in Taiyuan China.

For instance, when aluminum was added to mouse cortical neurons grown in cell culture, the cells began to die. By adding inhibitors of apoptosis (zVAD-fmk), of autophagy (3-methyladenin, 3-MA), or of necroptosis (necrostatin-1, Nec-1), investigators showed that all treatments enhanced cell viability although Nec-1 demonstrated the strongest protection. Using fluorescent microscopy, in which surviving neural cells stain green, apoptotic cells stain orange, and necrotic cells stain red, the investigators demonstrated Al-induced cell death as well as dose-dependent reduction of necroptosis with Nec-1.

When aluminum was injected into the cerebral ventricles of living mice, brain tissue analysis revealed shrunken and abnormal-looking neurons. When Nec-1 was injected simultaneously with aluminum into the ventricles, more surviving neurons could be seen, especially when higher doses of Nec-1 were used. When the investigators measured cell death-related proteins in the brain, a marker protein of necroptosis known as RIP1 showed the most changes, compared to marker proteins of apoptosis or autophagy. Similar findings were found for Alzheimer-related proteins: aluminum exposure increased the expression of mGluR2, mGluR5, Aβ, and Tau levels while Nec-1 treatment resulted in dose-dependent reductions of these protein levels.

Noting that “progressive cell loss in specific neuronal populations associated with typical learning and memory dysfunction is a pathological hallmark of neurodegenerative disorders, especially in AD,” principal investigator Qiao Niu, MD, PhD, Director, Department of Occupational Health and Director, Institute of Preventive Medicine, Shanxi Medical University, and the team evaluated learning and memory in mice using the Morris Water Maze test. Al-treated mice performed poorly on the test and performance significantly improved if the mice were treated with Nec-1. Interestingly, if Nec-1 treatment was delayed for 2, 4, or 8 hours after the aluminum was introduced, Nec-1 had a protective effect less than simultaneous administration. Impaired cognitive performance was also correlated with reduced mGluR2 and mGluR5 protein in the cortex. “Nec-1, in addition to its use as a therapeutic agent for cell death, might therefore be of use in slowing the progression of the cognitive deficits associated with neuronal degeneration,” says Dr. Niu.

The study demonstrates that Nec-1 may be useful for future prevention of and therapy for neurodegenerative disorders.

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151st Health Research Report 22 MAR 2013

In this Issue:

Folic acid lowers risk of autism

Bitter melon juice prevents pancreatic cancer in mouse models

Study: Probiotics reduce stress-induced intestinal flare-ups

Green tea, coffee may help lower stroke risk

How oils and fats regulate feeling of satiety

Study Shows How Vitamin E Can Help Prevent Cancer

New study highlights strong anti-cancer properties of soybeans

Explaining how extra virgin olive oil protects against Alzheimer’s disease

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Health Research Report

151st Issue Date 22 Mar 2013

Compiled By Ralph Turchiano

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Green tea extract interferes with the formation of amyloid plaques in Alzheimer’s disease

Contact: Laura J. Williams laurajw@umich.edu 734-615-4862 University of Michigan

ANN ARBOR—Researchers at the University of Michigan have found a new potential benefit of a molecule in green tea: preventing the misfolding of specific proteins in the brain.

The aggregation of these proteins, called metal-associated amyloids, is associated with Alzheimer’s disease and other neurodegenerative conditions.

A paper published recently in the Proceedings of the National Academy of Sciences explained how U-M Life Sciences Institute faculty member Mi Hee Lim and an interdisciplinary team of researchers used green tea extract to control the generation of metal-associated amyloid-β aggregates associated with Alzheimer’s disease in the lab.

The specific molecule in green tea, (—)-epigallocatechin-3-gallate, also known as EGCG, prevented aggregate formation and broke down existing aggregate structures in the proteins that contained metals—specifically copper, iron and zinc.

“A lot of people are very excited about this molecule,” said Lim, noting that the EGCG and other flavonoids in natural products have long been established as powerful antioxidants. “We used a multidisciplinary approach. This is the first example of structure-centric, multidisciplinary investigations by three principal investigators with three different areas of expertise.”

The research team included chemists, biochemists and biophysicists.

While many researchers are investigating small molecules and metal-associated amyloids, most are looking from a limited perspective, said Lim, assistant professor of chemistry and research assistant professor at the Life Sciences Institute, where her lab is located and her research is conducted.

“But we believe you have to have a lot of approaches working together, because the brain is very complex,” she said.

The PNAS paper was a starting point, Lim said, and her team’s next step is to “tweak” the molecule and then test its ability to interfere with plaque formation in fruit flies.

“We want to modify them for the brain, specifically to interfere with the plaques associated with Alzheimer’s,” she said.

Lim plans to collaborate with Bing Ye, a neurobiologist in the LSI. Together, the researchers will test the new molecule’s power to inhibit potential toxicity of aggregates containing proteins and metals in fruit flies.

###

Other authors of the paper, all from U-M, are: Sanghyun Lee and Jung-Suk Choi of the Life Sciences Institute; Alaina DeToma, Suk-Joon Hyung, Akiko Kochi and Brandon Ruotoloa of the Department of Chemistry; and Jeffrey Brender, Ayyalusamy Ramamoorthy and Subramanian Vivekanandan of the Department of Chemistry and Biophysics.

The work was supported by the National Institutes of Health, Alzheimer’s Association, Alzheimer’s Art Quilt Initiative, American Heart Association, and a Graduate Research Fellowship from the National Science Foundation Study: http://www.pnas.org/content/early/2013/02/19/1220326110.abstract

148th Health Research Report 08 FEB 2013 – Highlights

In this Issue:

1.     Skin, soft tissue infections succumb to blue light
2.     Silibinin, found in milk thistle, protects against UV-induced skin cancer
3.     20 hours of TV a week almost halves sperm count
4.     Sunlight may help ward off rheumatoid arthritis in women
5.     Low vitamin D levels may increase risk of Type 1 diabetes
6.     Green tea and red wine extracts interrupt Alzheimer’s disease pathway in cells
7.     Olive oil component alleviates intestinal ischemia and reperfusion
8.     Some omega-3 oils better than others for protection against liver disease
9.     Vitamin D, omega-3 may help clear amyloid plaques found in Alzheimer’s
10.  Fish oil may protect dialysis patients from sudden cardiac death
11.  Zinc helps against infection by tapping brakes in immune response
 
Articles here and at:
 
healthresearchreport.me

Vitamin D, omega-3 may help clear amyloid plaques found in Alzheimer’s

Contact: Rachel Champeau rchampeau@mednet.ucla.edu 310-794-2270 University of California – Los Angeles Health Sciences

A team of academic researchers has pinpointed how vitamin D3 and omega-3 fatty acids may enhance the immune system’s ability to clear the brain of amyloid plaques, one of the hallmarks of Alzheimer’s disease.

In a small pilot study published in the Feb. 5 issue of the Journal of Alzheimer’s Disease, the scientists identified key genes and signaling networks regulated by vitamin D3 and the omega-3 fatty acid DHA (docosahexaenoic acid) that may help control inflammation and improve plaque clearance.

Previous laboratory work by the team helped clarify key mechanisms involved in helping vitamin D3 clear amyloid-beta, the abnormal protein found in the plaque. The new study extends the previous findings with vitamin D3 and highlights the role of omega-3 DHA.

“Our new study sheds further light on a possible role for nutritional substances such as vitamin D3 and omega-3 in boosting immunity to help fight Alzheimer’s,” said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA.

For the study, scientists drew blood samples from both Alzheimer’s patients and healthy controls, then isolated critical immune cells called macrophages from the blood. Macrophages are responsible for gobbling up amyloid-beta and other waste products in the brain and body.

The team incubated the immune cells overnight with amyloid-beta. They added either an active form of vitamin D3 called 1alpha,25–dihydroxyvitamin D3 or an active form of the omega-3 fatty acid DHA called resolvin D1 to some of the cells to gauge the effect they had on inflammation and amyloid-beta absorption.

Both 1alpha, 25-dihydroxyvitamin D3 and resolvin D1 improved the ability of the Alzheimer’s disease patients’ macrophages to gobble-up amyloid-beta, and they inhibited the cell death that is induced by amyloid-beta. Researchers observed that each nutrition molecule utilized different receptors and common signaling pathways to do this.

Previous work by the team, based on the function of Alzheimer’s patients’ macrophages, showed that there are two groups of patients and macrophages. In the current study, researchers found that the macrophages of the Alzheimer’s patients differentially expressed inflammatory genes, compared with the healthy controls, and that two distinct transcription patterns were found that further define the two groups: Group 1 had an increased transcription of inflammatory genes, while Group 2 had decreased transcription. Transcription is the first step leading to gene expression.

“Further study may help us identify if these two distinct transcription patterns of inflammatory genes could possibly distinguish either two stages or two types of Alzheimer’s disease,” said study author Mathew Mizwicki, an assistant researcher at the David Geffen School of Medicine at UCLA.

While researchers found that 1alpha,25-dihydroxyvitamin D3 and resolvin D1 greatly improved the clearance of amyloid-beta by macrophages in patients in both groups, they discovered subtleties in the effects the two substances had on the expression of inflammatory genes in the two groups. In Group 1, the increased-inflammation group, macrophages showed a decrease of inflammatory activation; in Group 2,  macrophages showed an increase of the inflammatory genes IL1 and TLRs when either 1alpha,25-Dihydroxyvitamin D3 or resolvin D1 were added.

More study is needed, Fiala said, but these differences could be associated with the severity of patients’ nutritional and/or metabolic deficiencies of vitamin D3 and DHA, as well as the omega-3 fatty acid EPA (eicosapentaenoic acid).

“We may find that we need to carefully balance the supplementation with vitamin D3 and omega-3 fatty acids, depending on each patient in order to help promote efficient clearing of amyloid-beta,” Fiala said. “This is a first step in understanding what form and in which patients these nutrition substances might work best.”

According to Fiala, an active (not oxidized) form of omega-3 DHA, which is the precursor of the resolvin D1 used in this study, may work better than more commercially available forms of DHA, which generally are not protected against the oxidation that can render a molecule inactive.

The next step is a larger study to help confirm the findings, as well as a clinical trial with omega-3 DHA, the researchers said.

###

The Alzheimer’s Association contributed to the initial phase of the study. Fiala is a consultant for the Smartfish Company that is producing a drink with an active form of omega-3 DHA.

Additional study authors include Guanghao Liu, Larry Magpantay, James Sayre, Avi Siani, Michelle Mahanian, Rachel Weitzman, Eric Hayden, Mark J. Rosenthal, Ilka Nemere, John Ringman and David B. Teplow.

For more news, visit the UCLA Newsroom and follow us on Twitter

Green tea and red wine extracts interrupt Alzheimer’s disease pathway in cells

Contact: Chris Bunting c.j.bunting@leeds.ac.uk 44-113-343-2049 University of Leeds

Natural chemicals found in green tea and red wine may disrupt a key step of the Alzheimer’s disease pathway, according to new research from the University of Leeds.

In early-stage laboratory experiments, the researchers identified the process which allows harmful clumps of protein to latch on to brain cells, causing them to die. They were able to interrupt this pathway using the purified extracts of EGCG from green tea and resveratrol from red wine.

The findings, published in the Journal of Biological Chemistry, offer potential new targets for developing drugs to treat Alzheimer’s disease, which affects some 800,000 people in the UK alone, and for which there is currently no cure.

“This is an important step in increasing our understanding of the cause and progression of Alzheimer’s disease,” says lead researcher Professor Nigel Hooper of the University’s Faculty of Biological Sciences. “It’s a misconception that Alzheimer’s is a natural part of ageing; it’s a disease that we believe can ultimately be cured through finding new opportunities for drug targets like this.”

Alzheimer’s disease is characterised by a distinct build-up of amyloid protein in the brain, which clumps together to form toxic, sticky balls of varying shapes. These amyloid balls  latch on to the surface of nerve cells in the brain by attaching to proteins on the cell surface called prions, causing the nerve cells to malfunction and eventually die.

“We wanted to investigate whether the precise shape of the amyloid balls is essential for them to attach to the prion receptors, like the way a baseball fits snugly into its glove,” says co-author Dr Jo Rushworth. “And if so, we wanted to see if we could prevent the amyloid balls binding to prion by altering their shape, as this would stop the cells from dying.”

The team formed amyloid balls in a test tube and added them to human and animal brain cells. Professor Hooper said: “When we added the extracts from red wine and green tea, which recent research has shown to re-shape amyloid proteins, the amyloid balls no longer harmed the nerve cells. We saw that this was because their shape was distorted, so they could no longer bind to prion and disrupt cell function.

“We also showed, for the first time, that when amyloid balls stick to prion, it triggers the production of even more amyloid, in a deadly vicious cycle,” he added.

Professor Hooper says that the team’s next steps are to understand exactly how the amyloid-prion interaction kills off neurons.

“I’m certain that this will increase our understanding of Alzheimer’s disease even further, with the potential to reveal yet more drug targets,” he said.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, which part-funded the study, said: “Understanding the causes of Alzheimer’s is vital if we are to find a way of stopping the disease in its tracks. While these early-stage results should not be a signal for people to stock up on green tea and red wine, they could provide an important new lead in the search for new and effective treatments. With half a million people affected by Alzheimer’s in the UK, we urgently need treatments that can halt the disease – that means it’s crucial to invest in research to take results like these from the lab bench to the clinic.”

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The research was funded by the Wellcome Trust, Alzheimer’s Research UK and the Medical Research Council.

Further information

For interviews, please contact Chris Bunting, Press Officer, University of Leeds; phone 0113 343 2049, email c.j.bunting@leeds.ac.uk

The Full Paper:  Jo V. Rushworth, Heledd H. Griffiths, Nicole T. Watt and Nigel M. Hooper, ‘Prion protein-mediated neurotoxity of amyloid-β oligomers requires lipid rafts and the transmembrane LRP1,’ Journal of Biological Chemistry [DOI:10.1074/jbc.M112.400358] is available at http://www.jbc.org/content/early/2013/02/06/jbc.M112.400358.full.pdf+html from 6pm (EST), February 5.  Copies of the paper are available on request from the University of Leeds press office.

Notes for editors:

1. Nigel Hooper is Professor of Biochemistry at the University of Leeds. Further information about his research can be found here: http://www.fbs.leeds.ac.uk/staff/profile.php?un=bmbnmh

2. Alzheimer’s disease is the most common form of dementia, costing the UK economy £23 billion per year.  One in three people aged over 65 are expected to die with a form of dementia and 163,000 new cases are diagnosed in England and Wales each year. Worldwide, more than 35 million people are estimated to have dementia. (Source: www.alzheimersresearchuk.org )

3. University of Leeds, Faculty of Biological Sciences

The Faculty of Biological Sciences at the University of Leeds is one of the largest in the UK, with over 110 academic staff and over 400 postdoctoral fellows and postgraduate students. The Faculty is ranked 4th in the UK (Nature Journal, 457 (2009) doi:10.1038/457013a) based on results of the 2008 Research Assessment Exercise (RAE).  The RAE feedback noted that “virtually all outputs were assessed as being recognized internationally, with many (60%) being internationally excellent or world-leading” in quality. The Faculty’s research grant portfolio totals some £53M and funders include charities, research councils, the European Union and industry.  www.fbs.leeds.ac.uk

4. The Wellcome Trust is a global charitable foundation dedicated to achieving extraordinary improvements in human and animal health. It supports the brightest minds in biomedical research and the medical humanities. The Trust’s breadth of support includes public engagement, education and the application of research to improve health. It is independent of both political and commercial interests. www.wellcome.ac.uk

5. Alzheimer’s Research UK is the UK’s leading charity specialising in finding preventions, treatments and a cure for dementia. We are currently supporting dementia research projects worth over £20 million in leading Universities across the UK. To help us defeat dementia, donate today by visiting www.alzheimersresearchuk.org or calling 01223 843899.

6. For almost 100 years the Medical Research Council has improved the health of people in the UK and around the world by supporting the highest quality science. The MRC invests in world-class scientists. It has produced 29 Nobel Prize winners and sustains a flourishing environment for internationally recognised research. The MRC focuses on making an impact and provides the financial muscle and scientific expertise behind medical breakthroughs, including the first antibiotic penicillin, the structure of DNA and the lethal link between smoking and cancer. Today MRC funded scientists tackle research into the major health challenges of the 21st century. www.mrc.ac.uk

Low Testosterone Linked to Alzheimer’s Disease

2010 study posted for filing

SLU Geriatrician Collaborates on Year-Long Study of Chinese Older Men

ST. LOUIS — Low levels of the male sex hormone, testosterone, in older men is associated with the onset of Alzheimer’s disease, according to research by a team that includes a Saint Louis University scientist.

John Morley, M.D.

“Having low testosterone may make you more vulnerable to Alzheimer’s disease,” said John E. Morley, M.D., director of the division of geriatric medicine at Saint Louis University and a study co-investigator. “The take-home message is we should pay more attention to low testosterone, particularly in people who have memory problems or other signs of cognitive impairment.”

The study was published electronically prior to its print publication in the Journal of Alzheimer’s Disease and led by Leung-Wing Chu, M.D., who is chief of the division of geriatric medicine at Queen Mary Hospital at the University of Hong Kong.

Researchers studied 153 Chinese men who were recruited from social centers. They were at least 55 years and older, lived in the community and didn’t have dementia. Of those men, 47 had mild cognitive impairment – or problems with clear thinking and memory loss.

Within a year, 10 men who all were part of the cognitively impaired group developed probable Alzheimer’s disease. These men also had low testosterone in their body tissues; elevated levels of the ApoE 4 (apolipoprotein E) protein, which is correlated with a higher risk of Alzheimer’s disease; and high blood pressure.

“It’s a very exciting study because we’ve shown that a low level of testosterone is one of the risk factors for Alzheimer’s disease,” Morley said.

The findings corroborate findings in previous studies of older Caucasian men that show low testosterone is associated with impaired thinking and Alzheimer’s disease. They suggest that testosterone may have a protective value against Alzheimer’s disease.

The next step, Morley said, is to conduct a large-scale study that investigates the use of testosterone in preventing Alzheimer’s disease. Morley and his co-authors advocate studying the effectiveness of testosterone replacement in older men who have both mild memory problems and low testosterone in staving off Alzheimer’s disease.

Liver defect likely cause of DHA deficiency in Alzheimer’s patients, UCI study finds

2010 study posted for filing

Contact: Janet Wilson janethw@uci.edu 949-824-3969 University of California – Irvine

Low levels of the omega-3 fatty acid may contribute to the neurodegenerative disease

Irvine, Calif. — UC Irvine researchers have discovered that markedly depleted amounts of an omega-3 fatty acid in brain tissue samples from Alzheimer’s patients may be due to the liver’s inability to produce the complex fat, also contained in fish-oil supplements.

Low levels of docosahexaenoic acid, or DHA, have been associated with the chronic neurodegenerative disease affecting millions of Americans, but no cause had been identified.

In postmortem liver tissue from Alzheimer’s patients, the UCI team found a defect in the organ’s ability to make DHA from shorter molecules present in leafy plants and other foods. Previous studies have shown that most brain DHA is manufactured in the liver.

Non-Alzheimer’s livers did not have this defect, said Daniele Piomelli, the Louise Turner Arnold Chair in the Neurosciences and director of the Center for Drug Discovery at UCI, who led the research with Giuseppe Astarita, project scientist in pharmacology.

“We all know Alzheimer’s is a brain disease, but our findings – which were totally unexpected – show that a problem with liver fat metabolism can make people more vulnerable,” Piomelli said. “They also suggest a reason why clinical trials in which Alzheimer’s patients are given omega-3 fatty acids to improve cognitive skills have had mixed results.”

The study appears Sept. 8 in the open-access, peer-reviewed journal PLoS ONE.

DHA occurs naturally in cold-water fatty fish and seaweed. It is essential for the proper functioning of adult human brains and for the development of our nervous system and vision during the first six months of life. Omega-3 fatty acids are also part of a healthy diet that helps lower risk of heart disease.

“Additionally, we found that the greater the amount of Alzheimer’s-related cognitive problems experienced in life by the patients, the lower were their liver DHA levels,” Astarita said. “So we do see a connection.”

Piomelli added that the results point to new diagnostic and dietary approaches to Alzheimer’s: Specific blood lipid profile tests might identify at-risk persons, and dietary supplements with a chemically enhanced form of DHA may benefit early-stage patients.

“Our research isn’t advocating that liver metabolism is a key to Alzheimer’s,” he noted. “The factors causing the disease are many and complex, but we feel this is another piece in the Alzheimer’s puzzle.”

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Carl Cotman, Kwang-Mook Jung, Nicole C. Berchtold, Vinh Q. Nguyen and Daniel L. Gillen of UCI’s Institute for Memory Impairments and Neurological Disorders contributed to the study, along with Elizabeth Head of the University of Kentucky’s Sanders-Brown Center on Aging.

About the University of California, Irvine: Founded in 1965, UCI is a top-ranked university dedicated to research, scholarship and community service. Led by Chancellor Michael Drake since 2005, UCI is among the most dynamic campuses in the University of California system, with nearly 28,000 undergraduate and graduate students, 1,100 faculty and 9,000 staff. Orange County’s largest employer, UCI contributes an annual economic impact of $3.9 billion. For more UCI news, visit www.today.uci.edu.

News Radio: UCI maintains on campus an ISDN line for conducting interviews with its faculty and experts. Use of this line is available for a fee to radio news programs/stations that wish to interview UCI faculty and experts. Use of the ISDN line is subject to availability and approval by the university.

UCI maintains an online directory of faculty available as experts to the media. To access, visit http://www.today.uci.edu/experts. For UCI breaking news, visit www.zotwire.uci.edu.

Healthy diet could slow or reverse early effects of Alzheimer’s disease

2010 study posted for filing

Contact: Preston M. Moretz pmoretz@temple.edu 215-204-4380 Temple University

Patients in the early to moderate stages of Alzheimer’s Disease could have their cognitive impairment slowed or even reversed by switching to a healthier diet, according to researchers at Temple University.

In a previous study [http://www.temple.edu/newsroom/2009_2010/12/stories/alzheimers.htm], researchers led by Domenico Praticò, an associate professor of pharmacology in Temple’s School of Medicine, demonstrated that a diet rich in methionine could increase the risk of developing Alzheimer’s Disease. Methionine is an amino acid typically found in red meats, fish, beans, eggs, garlic, lentils, onions, yogurt and seeds.

“The question we asked now as a follow-up is if, for whatever reason, you had made bad choices in your diet, is there a chance you can slow down or even reverse the disease or is it too late — that there is nothing you could do,” said Praticò.

As in the previous study, the researchers fed one group of mice a diet high in methionine and another group a regular, healthy diet. After five months, they split the group receiving the methionine-rich diet into two, with one group continuing the amino-heavy diet while the second switched to the healthy diet for an additional two months.

“At the end of the study, when we looked at these mice, what we found — very surprisingly — was that switching to a more healthy diet reversed the cognitive impairment that had built up over the first three months of eating the methionine-rich diet,” said Praticò. “This improvement was associated with less amyloid plaques — another sign of the disease — in their brains.

Pratico said that the cognitive impairment that had been observed in the mice after three months on the methionine-rich diet was completely reversed after two months on the healthier diet, and they were now able to function normally.

“We believe this finding shows that, even if you suffer from the early effects of MCI or Alzheimer’s, switching to a healthier diet that is lower in methionine could be helpful in that memory capacity could be improved,” he said.

Pratico stressed that this was not a drug therapy for curing MCI or Alzheimer’s, but that it did demonstrate that a lifestyle change such as diet can improve some of the impairments that have already occurred in the brain.

“What it tells us is that the brain has this plasticity to reverse a lot of the bad things that have occurred; the ability to recoup a lot of things such as memory that were apparently lost, but obviously not totally lost,” he said.

Pratico also emphasized that the researchers believe that in addition to switching to a healthy diet, patients diagnosed with MCI or Alzheimer’s also need a regiment of physical as well as mental exercises.

“This combination won’t cure you, but we believe, as we saw in this study, that it will be able to slow down or even possibly reverse the effects on the cognitive impairment,” he said.

###

The study, “Normalization of hyperhomocysteinemia improves cognitive deficits and ameliorates brain amyloidosis of a transgenic mouse model of Alzheimer’s disease,” is being published in the Journal of the Federation of American Societies for Experimental Biology (http://www.fasebj.org/). It was funded by a grant from the National Institutes of Health.

Copies of this study are available to working journalists and may be obtained by contacting Preston M. Moretz in Temple’s Office of University Communications at pmoretz@temple.edu.

Key nutrient in maternal diet promises ‘dramatic’ improvements for people with Down syndrome ( Choline )

2010 study posted for filing

Contact: John Carberry jjc338@cornell.edu 607-255-5353 Cornell University

ITHACA, N.Y. – A nutrient found in egg yolks, liver and cauliflower taken by mothers during pregnancy and nursing may offer lifelong “dramatic” health benefits to people with Down syndrome .

A new study done at Cornell University and published June 2 in the peer-reviewed journal Behavioral Neuroscience found that more choline during pregnancy and nursing could provide lasting cognitive and emotional benefits to people with Down syndrome. The work indicated greater maternal levels of the essential nutrient also could protect against neurodegenerative conditions such as Alzheimer’s disease.

“We found that supplementing the maternal diet with additional choline resulted in dramatic improvements in attention and some normalization of emotion regulation in a mouse model of Down syndrome,” said lead author Barbara Strupp, professor of nutritional sciences and of psychology.

In addition to mental retardation, Down syndrome individuals often experience dementia in middle age as a result of brain neuron atrophy similar to that suffered by people with Alzheimer’s disease. Strupp said the improved mental abilities found in the Down syndrome mice following maternal choline supplements could indicate protection from such neurodegeneration “in the population at large.”

Strupp and her co-authors tested Down syndrome-model mice born from mothers that were fed a normal diet versus those given choline supplements during their three-week pregnancy and three-week lactation period. They also examined normal mice born from mothers with and without additional choline. The choline-supplemented mothers received about 4.5 times more choline (roughly comparable to levels at the higher range of human intake) than unsupplemented mothers.

Beginning at 6 months of age, the mice performed a series of behavioral tasks over a period of about six months to assess their impulsivity, attention span, emotional control and other mental abilities. The researchers found the unsupplemented Down syndrome-model mice became more agitated after a mistake than normal mice, jumping repeatedly and taking longer to initiate the next trial. The choline-supplemented Down syndrome-model mice showed partial improvement in these areas.

“I’m impressed by the magnitude of the cognitive benefits seen in the Down syndrome-model mice,” Strupp said. “Moreover, these are clearly lasting cognitive improvements, seen many months after the period of choline supplementation.”

Strupp said the results are consistent with studies by other researchers that found increased maternal choline intake improves offspring cognitive abilities in rats. However, this is the first study to evaluate the effects of maternal choline supplementation in a rodent model of Down syndrome.

Previous studies of humans and laboratory animals have shown that supplementing the diets of adults with choline has proven to be largely ineffective in improving cognition.

“Although the precise mechanism is unknown, these lasting beneficial effects of choline observed in the present study are likely to be limited to increased intake during very early development,” Strupp said.

###

The study, funded in part by the National Institutes of Health, was part of the dissertation of Cornell doctoral candidate Jisook Moon. Other Cornell collaborators included Myla Strawderman, research associate in nutritional sciences, and David Levitsky, professor of nutrition and psychology. Strupp and collaborators have received additional NIH funding to study the neural mechanisms underlying the results observed in this study.

Obesity gene, carried by more than a third of the US population, leads to brain tissue loss

2010 study posted for filing

Contact: Mark Wheeler mwheeler@mednet.ucla.edu 310-794-2265 University of California – Los Angeles

Three years ago, geneticists reported the startling discovery that nearly half of all people in the U.S. with European ancestry carry a variant of the fat mass and obesity associated (FTO) gene, which causes them to gain weight — from three to seven pounds, on average — but worse, puts them at risk for obesity.

Now, UCLA researchers have found that the same gene allele, which is also carried by roughly one-quarter of U.S. Hispanics, 15 percent of African Americans and 15 percent of Asian Americans, may have another deleterious effect.

Reporting in the early online edition of the journal Proceedings of the National Academy of Sciences, senior study author Paul Thompson, a UCLA professor of neurology; lead authors April Ho and Jason Stein, graduate students in Thompson’s lab; and colleagues found that the FTO variant is also associated with a loss of brain tissue. This puts more than a third of the U.S. population at risk for a variety of diseases, such as Alzheimer’s.

Using magnetic resonance imaging, the researchers generated three-dimensional “maps” of brain volume differences in 206 healthy elderly subjects drawn from 58 sites in the U.S. as part of the Alzheimer’s Disease Neuroimaging Initiative, a large, five-year study aimed at better understanding factors that help the brain resist disease as it ages.

They found that there was consistently less tissue in the brains of those who carry the FTO allele, compared with non-carriers. Individuals with the “bad” version of the FTO gene had an average of 8 percent less tissue in the frontal lobes, the “command center” of the brain, and 12 percent less in the occipital lobes, areas in the back of the brain responsible for vision and perception. Further, the brain differences could not be directly attributed to other obesity-related factors such as cholesterol levels, diabetes or high blood pressure.

Thompson called the findings worrying and mysterious.

“The results are curious. If you have the bad FTO gene, your weight affects your brain adversely in terms of tissue loss,” he said. “If you don’t carry FTO, higher body weight doesn’t translate into brain deficits; in fact, it has nothing to do with it. This is a very mysterious, widespread gene.”

People who carry this specific DNA sequence are heavier on average, and their waist circumference is half an inch bigger.

This is a large percentage of the population, said Thompson, who is also a member of UCLA’s Brain Research Institute and the UCLA Laboratory of Neuro Imaging.

“This is a shocking finding. Any loss of brain tissue puts you at greater risk for functional decline,” he said. “The risk gene divides the world into two camps ― those who have the FTO allele and those who don’t.”

But the news is not necessarily completely negative, Thompson said, because “carriers of the risk gene can exercise and eat healthily to resist both obesity and brain decline.”

Thompson sees both a public health message and a science message in this finding.

“Half of the world carries this dangerous gene. But a healthy lifestyle will counteract the risk of brain loss, whether you carry the gene or not. So it’s vital to boost your brain health by being physically active and eating a balanced diet,” he said.

And from a scientific standpoint, he said, “the gene discovery will help to develop and fine tune the anti-dementia drugs being developed to combat brain aging.”

###

Funding for the study came from the National Institutes of Health and from private industry. The authors report no conflict of interest.

The UCLA Department of Neurology encompasses more than a dozen research, clinical and teaching programs that cover brain mapping and neuroimaging, movement disorders, Alzheimer’s disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranks first among its peers nationwide in National Institutes of Health funding.

For more news, visit the UCLA Newsroom and follow us on Twitter.

80th Health Research Report 22 APR 2010 : Reconstruction

Editors Top Five:

1. Vitamin K May Protect Against Developing Non-Hodgkin Lymphoma, Say Mayo Clinic Researchers

2. First evidence that chitosan could repair spinal damage

3. Over half of women in abusive relationships still saw their male partners as dependable

4. Why are allergies increasing?

5. Health, life insurers hold $1.88 billion in fast-food stocks: AJPH article

In this issue:

1. Stress hormones accelerate tumor growth
 
2. Study identifies food combination associated with reduced Alzheimer’s disease risk
 
3. Over half of women in abusive relationships still saw their male partners as dependable
 
4. U of I study: Lack of omega-6 fatty acid linked to severe dermatitis
 
5. U of I study: Lack of omega-3 fatty acid linked to male infertility(DHA)
 
6. Fear of getting fat seen in healthy women’s brain scans
 
7. Why are allergies increasing?
 
8. Diet alone will not likely lead to significant weight loss
 
9. BRAIN INFECTION FROM TAPEWORM “SERIOUS HEALTH CONCERN”
 
10. Health, life insurers hold $1.88 billion in fast-food stocks: AJPH article
 
11. Diet high in B-vitamins lowers heart risks in Japanese study
 
12. Study shows potential benefit of dark chocolate for liver disease patients
 
13. Low vitamin D levels associated with more asthma symptoms and medication use
 
14. First evidence that chitosan could repair spinal damage
 
15. Vitamin and calcium supplements may reduce breast cancer risk
 
16. Meat, especially if it’s well done, may increase risk of bladder cancer
 
17. Substance in breast milk kills cancer cells
 
18. Are doctors missing depression medication side effects?
 
19. Vitamin K May Protect Against Developing Non-Hodgkin Lymphoma, Say Mayo Clinic Researchers
 
20. Obesity gene, carried by more than a third of the U.S. population, leads to brain tissue loss

Public release date: 12-Apr-2010

Stress hormones accelerate tumor growth

Chronic stress has recently been implicated as a factor that may accelerate the growth of tumors. However, the mechanisms underlying this effect have not been determined. But now, Anil Sood and colleagues, at the University of Texas MD Anderson Cancer Center, Houston, have generated data using human ovarian cancer cell lines and tumor specimens that indicate that stress hormones, especially norepinephrine and epinephrine, can contribute to tumor progression in patients with ovarian cancer. They therefore suggest that targeting stress hormones and the signaling pathways that they activate might be of benefit to individuals with cancer.

Anoikis is the process by which cells are triggered to die when separated from their surrounding matrix and neighboring cells. Tumor cells that spread to other sites somehow escape anoikis. In the study, exposure of human ovarian cancer cells lines to either of the stress hormones norepinephrine or epinephrine protected them from anoikis. Similarly, in a mouse model of ovarian cancer, restraint stress and the associated increases in norepinephrine and epinephrine protected the tumor cells from anoikis and promoted their growth. This effect was associated with activation of the protein FAK. The clinical significance of these data was highlighted by the observation that in human ovarian cancer patients, behavioral states related to greater stress hormone activity were associated with higher levels of activated FAK, which was in turn linked to substantially accelerated mortality.

Public release date: 12-Apr-2010

Study identifies food combination associated with reduced Alzheimer’s disease risk

Individuals whose diet includes more salad dressing, nuts, fish, poultry and certain fruits and vegetables and fewer high-fat dairy products, red meats, organ meats and butter appear less likely to develop Alzheimer’s disease, according to a report posted online today that will appear in the June print issue of Archives of Neurology, one of the JAMA/Archives journals.

“Epidemiological evidence linking diet, one of the most important modifiable environmental factors, and risk of Alzheimer’s disease is rapidly increasing,” the authors write as background information in the article. “However, current literature regarding the impact of individual nutrients or food items on Alzheimer’s disease risk is inconsistent, partly because humans eat meals with complex combinations of nutrients or food items that are likely to be synergistic.”

Yian Gu, Ph.D., of Columbia University Medical Center, New York, and colleagues studied 2,148 older adults (age 65 and older) without dementia living in New York. Participants provided information about their diets and were assessed for the development of dementia every 1.5 years for an average of four years. Several dietary patterns were identified with varying levels of seven nutrients previously shown to be associated with Alzheimer’s disease risk: saturated fatty acids, monounsaturated fatty acids, omega-3 fatty acids, omega-6 fatty acids, vitamin E, vitamin B12 and folate.

During the follow-up, 253 individuals developed Alzheimer’s disease. One dietary pattern was significantly associated with a reduced risk of the disease. This pattern involved high intakes of salad dressing, nuts, fish, tomatoes, poultry, fruits and cruciferous and dark and green leafy vegetables and low intakes of high-fat dairy, red meat, organ meat and butter.

The combination of nutrients in the low-risk dietary pattern reflect multiple pathways in the development of Alzheimer’s disease, the authors note. “For example, vitamin B12 and folate are homocysteine-related vitamins that may have an impact on Alzheimer’s disease via their ability of reducing circulating homocysteine levels, vitamin E might prevent Alzheimer’s disease via its strong antioxidant effect and fatty acids may be related to dementia and cognitive function through atherosclerosis, thrombosis or inflammation via an effect on brain development and membrane functioning or via accumulation of beta-amyloid,” they write.

“Our findings provide support for further exploration of food combination–based dietary behavior for the prevention of this important public health problem,” they conclude.

Public release date: 12-Apr-2010

Over half of women in abusive relationships still saw their male partners as dependable

New study based on women’s self-reports suggests a subtype of men — categorized as ‘dependable yet abusive’ — is most common

TORONTO, Ont., April 12, 2010— It’s well known that many women remain in abusive relationships with their male partners. A new study by researchers in Toronto and New York suggests that many who live with chronic psychological abuse still see certain positive traits in their abusers—such as dependability and being affectionate—which may partly explain why they stay.

“We wanted to see whether survey information from women who were not currently seeking treatment or counseling for relationship abuse could be a reliable source for identifying specific types of male abusers,” says Patricia O’Campo, a social epidemiologist and director of the Centre for Research on Inner City Health at St. Michael’s Hospital in Toronto.

She adds that past research has underscored abused women’s personal evaluations of their intimate relationships—specifically, their commitment to the relationships and positive feelings about the abuser and/or the relationship—as critical in their decisions to continue or terminate abusive relationships. “We wanted to learn more,” says Dr. O’Campo, who co-authored the study with researchers from Adelphi University in Garden City, New York.

Using survey data from a project funded by the U.S. National Institute of Mental Health, the researchers explored the experiences of 611 urban-dwelling, low-income American women.

•Overall, 42.8% of those surveyed said they had been abused by their intimate male partners in the year preceding the survey.

•Psychological abuse was significantly more of an ongoing problem than physical abuse, while sexual abuse was reported as least common.

•A relatively small number of women (2.3%) perceived their partners as extremely controlling, while 1.2% reported that their partners engaged in extreme generally violent behaviours.

But a considerable number of women felt their abusive male partners still possessed some good qualities: more than half (54%) saw their partners as highly dependable, while one in five (21%) felt the men in their lives possessed significant positive traits (i.e., being affectionate).

Based on the survey findings, the researchers divided the male abusers into three groups: “Dependable, yet abusive” men (44% of the sample) had the lowest scores for controlling and generally violent behaviors, and the highest scores for dependability and positive traits. “Positive and controlling” men (38% of the sample) had moderately high scores for violence and also for dependability and positive traits. However, they were more controlling than men in the first group, displaying significantly higher levels of generally violent behaviours. “Dangerously abusive” men (18% of the sample) had the highest scores for violence, controlling behaviour and legal problems and the lowest scores for dependability and positive traits.

The researchers say their findings suggest there is value in studying the problem of male violence through the perceptions of abused women, including those who are currently “outside” the social services and legal systems designed to help them.

“The importance of listening to women’s voices cannot be highlighted enough and needs further exploration,” says O’Campo. “This is just one step toward potentially increasing our understanding of how to find additional ways to improve women’s safety.”

Ralph’s Note – A society that excepts this behavior as a norm. Is a society that no longer deserves to exit.

Public release date: 12-Apr-2010

U of I study: Lack of omega-6 fatty acid linked to severe dermatitis

URBANA –University of Illinois scientists have learned that a specific omega-6 fatty acid may be critical to maintaining skin health.

“In experiments with mice, we knocked out a gene responsible for an enzyme that helps the body to make arachidonic acid. Without arachidonic acid, the mice developed severe ulcerative dermatitis. The animals were very itchy, they scratched themselves continuously, and they developed a lot of bleeding sores,” said Manabu Nakamura, a U of I associate professor of food science and human nutrition.

When arachidonic acid was added to the animals’ diet, the itching went away, he said.

Nakamura’s team has been focusing on understanding the function of omega-3 and -6 fatty acids, and doctoral student Chad Stroud developed a mouse model to help them understand the physiological roles of these fats. By knocking out genes, they can create deficiencies of certain fats and learn about their functions.

“Knocking out a gene that enables the body to make the delta-6-desaturase enzyme has led to some surprising discoveries. In this instance, we learned that arachidonic acid is essential for healthy skin function. This new understanding may have implications for treating the flaky, itchy skin that sometimes develops without an attributable cause in infants,” he said.

Nakamura explained that our bodies make arachidonic acid from linoleic acid, an essential fatty acid that we must obtain through our diets. It is found mainly in vegetable oils.

Scientists have long attributed healthy skin function to linoleic acid, which is important because it provides the lipids that coat the outer layer of the skin, keeping the body from losing water and energy, which would retard growth, the scientist said.

But skin function seems to be more complicated than that. These itchy mice had plenty of linoleic acid. They just couldn’t convert it to arachidonic acid because the gene to make the necessary enzyme had been knocked out, he noted.

Arachidonic acid is also essential to the production of prostaglandins, compounds that can lead to inflammatory reactions and are important to immune function. Common painkillers like aspirin and ibuprofen work by inhibiting the conversion of arachidonic acid to prostaglandins.

“We usually think of inflammation as a bad thing, but in this case, prostaglandins prevented dermatitis, which is an inflammatory reaction. We measured prostaglandin levels in the animals’ skin, and when we fed arachidonic acid to the knockout mice, they resumed making these important chemical compounds,” he said.

Nakamura cautioned that there are still things they don’t understand about the function of this omega-6 fatty acid. “This new knowledge is a starting point in understanding the mechanisms that are involved, and we need to do more research at the cellular level.”

Public release date: 12-Apr-2010

U of I study: Lack of omega-3 fatty acid linked to male infertility(DHA)

URBANA – According to a University of Illinois study, omega-3 fatty acids may be good for more than heart health. A little-known omega-3 may have implications for treating male infertility.

“In our experiment, we used ‘knockout’ mice that lacked the gene responsible for an enzyme important in making docosahexaenoic acid (DHA). In the absence of DHA, male mice are basically infertile, producing few if any misshaped sperm that can’t get where they need to go,” said Manabu Nakamura, a U of I associate professor of food science and human nutrition.

“We looked at sperm count, shape, and motility and tested the breeding success rate, and the mice lacking DHA simply were not able to breed,” said Manuel Roqueta-Rivera, a U of I doctoral student who also worked on the study.

In the DHA-deficient knockout mice, sperm counts were extremely low. The sperm that were produced were round instead of elongated and they were unable to move well, he said.

But, when DHA was introduced into the diet, fertility was completely restored. “It was very striking. When we fed the mice DHA, all these abnormalities were prevented,” he said.

This is the first time that the importance of DHA to male fertility has been shown this directly, although some studies have suggested that male fertility patients with low sperm counts and less motile sperm tend to have low levels of this fatty acid.

The DHA study is part of the Nakamura team’s efforts to understand the function of the omega-3 and -6 fatty acids. As part of that work, they have developed a mouse model to help them understand a particular fat’s physiological role. By knocking out genes, they can create deficiencies of the fats they are interested in and learn about their functions.

“Knocking out the gene for the delta-6-desaturase enzyme has led to some surprising discoveries, including this one about the importance of DHA in sperm formation and mobility,” he said.

Nakamura said our body must make DHA from dietary alpha-linolenic acids, the parent compound of the omega-3 fatty acid family. Vegetable oils, including soybean and canola oil, are good sources of alpha-linolenic acid.

Nakamura’s team plans to continue focusing on this omega-3’s effects on fertility. But he cautioned that there are still things they don’t understand.

“We get hints from looking at sperm in the DHA-deficient animals about what type of pathology we may be looking at and why these polyunsaturated fatty acids are important. But we’re still at the starting point in understanding the mechanisms that are involved, and we need to do more research at the cellular level,” he said.

Public release date: 12-Apr-2010

Fear of getting fat seen in healthy women’s brain scans

A group of women in a new study seemed unlikely to have body image issues – at least their responses on a tried-and-true psychological screening presented no red flags.

That assessment changed when Brigham Young University researchers used MRI technology to observe what happened in the brain as these women viewed images of complete strangers.

If the stranger happened to be overweight and female, it surprisingly activated in women’s brains an area that processes identity and self-reflection. Men did not show signs of any self-reflection in similar situations.

“These women have no history of eating disorders and project an attitude that they don’t care about body image,” said Mark Allen, a BYU neuroscientist. “Yet under the surface is an anxiety about getting fat and the centrality of body image to self.”

Allen makes his report with grad student Tyler Owens and BYU psychology professor Diane Spangler in the May issue of the psychological journal Personality and Individual Differences.

Spangler and Allen collaborate on a long-term project to improve treatment of eating disorders by tracking progress with brain imaging. When anorexic and bulimic women view an overweight stranger, the brain’s self-reflection center – known as the medial prefrontal cortex – lights up in ways that suggest extreme unhappiness and in some cases, self-loathing.

The motivation for this new study was to establish a point of reference among a control group of women who scored in the healthy range on eating disorder diagnostic tests. Surprisingly, even this control group exhibited what Allen calls “sub-clinical” issues with body image.

Seeing that, Allen and Owens ran the experiments with a group of men for comparison.

“Although these women’s brain activity doesn’t look like full-blown eating disorders, they are much closer to it than men are,” Allen said.

Spangler says women are bombarded with messages that perpetuate the thin ideal, and the barrage changes how they view themselves.

“Many women learn that bodily appearance and thinness constitute what is important about them, and their brain responding reflects that,” Spangler said. “I think it is an unfortunate and false idea to learn about oneself and does put one at greater risk for eating and mood disorders.”

“It’s like the plant in my office,” she continued.“It has the potential to grow in any direction, but actually only grows in the direction of the window – the direction that receives the most reinforcement.”

Ralph’s Note – What is wrong with not desiring to be unhealthy?

Public release date: 13-Apr-2010

Why are allergies increasing?

Université de Montréal professor studies how probiotics can help

Montreal, April 13, 2010 – Allergies have become a widespread in developed countries: hay fever, eczema, hives and asthma are all increasingly prevalent. The reason? Excessive cleanliness is to blame according to Dr. Guy Delespesse, a professor at the Université de Montréal Faculty of Medicine.

Allergies can be caused by family history, air pollution, processed foods, stress, tobacco use, etc. Yet our limited exposure to bacteria concerns Dr. Delespesse, who is also director of the Laboratory for Allergy Research at the Centre hospitalier de l’Université de Montréal.

“There is an inverse relationship between the level of hygiene and the incidence of allergies and autoimmune diseases,” says Dr. Delespesse. “The more sterile the environment a child lives in, the higher the risk he or she will develop allergies or an immune problem in their lifetime.”

In 1980, 10 percent of the Western population suffered from allergies. Today, it is 30 percent. In 2010, one out of 10 children is said to be asthmatic and the mortality rate resulting from this affliction increased 28 percent between 1980 and 1994.

“It’s not just the prevalence but the gravity of the cases,” says Dr. Delespesse. “Regions in which the sanitary conditions have remained stable have also maintained a constant level of allergies and inflammatory diseases.”

“Allergies and other autoimmune diseases such as Type 1 diabetes and multiple sclerosis are the result of our immune system turning against us,” says Dr. Delespesse.

Why does this happen? “The bacteria in our digestive system are essential to digestion and also serve to educate our immune system. They teach it how to react to strange substances. This remains a key in the development of a child’s immune system.”

Although hygiene does reduce our exposure to harmful bacteria it also limits our exposure to beneficial microorganisms. As a result, the bacterial flora of our digestive system isn’t as rich and diversified as it used to be.

Dr. Delespesse recommends probiotics to enrich our intestinal flora. Probiotics are intestinal bacteria that have a beneficial impact on health. They’ve been used for decades to make yogurt. Probiotics have a proven effect on treating diarrhea, and studies are increasingly concluding similar benefits for the immune system and allergies.

“Consuming probiotics during pregnancy could help reduce allergies in the child,” says Dr. Delespesse. “They are not a miracle remedy, yet they are one of many elements that improve our diet and our health.”

Public release date: 13-Apr-2010

Diet alone will not likely lead to significant weight loss

PORTLAND, Ore – Newly-published research by scientists at Oregon Health & Science University demonstrates that simply reducing caloric intake is not enough to promote significant weight loss. This appears to be due to a natural compensatory mechanism that reduces a person’s physical activity in response to a reduction in calories. The research is published in the April edition of the American Journal of Physiology – Regulatory, Integrative and Comparative Physiology.

“In the midst of America’s obesity epidemic, physicians frequently advise their patients to reduce the number of calories they are consuming on a daily basis. This research shows that simply dieting will not likely cause substantial weight loss. Instead, diet and exercise must be combined to achieve this goal,” explained Judy Cameron Ph.D., a senior scientist at OHSU’s Oregon National Primate Research Center, and a professor of behavioral neuroscience and obstetrics & gynecology in the OHSU School of Medicine, as well as a professor of psychiatry at the University of Pittsburgh.

To conduct the research, Cameron and OHSU post-doctoral fellow Elinor Sullivan, Ph.D., studied 18 female rhesus macaque monkeys at the Oregon National Primate Research Center. The monkeys were placed on a high-fat diet for several years. They were then returned to a lower-fat diet (standard monkey food) with a 30 percent reduction in calories. For a one-month period, the monkeys’ weight and activity levels were closely tracked. Activity was tracked through the use of an activity monitor worn on a collar.

“Surprisingly, there was no significant weight loss at the end of the month,” explained Sullivan. “However, there was a significant change in the activity levels for these monkeys. Naturally occurring levels of physical activity for the animals began to diminish soon after the reduced-calorie diet began. When caloric intake was further reduced in a second month, physical activity in the monkeys diminished even further.”

A comparison group of three monkeys was fed a normal monkey diet and was trained to exercise for one hour daily on a treadmill. This comparison group did lose weight.

“This study demonstrates that there is a natural body mechanism which conserves energy in response to a reduction in calories. Food is not always plentiful for humans and animals and the body seems to have developed a strategy for responding to these fluctuations,” added Cameron. “These findings will assist medical professionals in advising their patients. It may also impact the development of community interventions to battle the childhood obesity epidemic and lead to programs that emphasize both diet and exercise.”

Public release date: 13-Apr-2010

BRAIN INFECTION FROM TAPEWORM “SERIOUS HEALTH CONCERN”

Increasing in Mexico and Bordering Southwestern States

MAYWOOD, Ill. — Tapeworm infections of the brain, which can cause epileptic seizures, appear to be increasing in Mexico and bordering southwestern states, Loyola University Health System researchers report.

In Mexico, up to 10 percent of the population may have the infection, neurocysticercosis. While many people never develop symptoms, neurocysticercosis nevertheless “remains a serious health concern, especially among the poor,” Loyola researchers wrote in the April issue of the journal Neurological Research.

Their article, “Management of Neurocysticercosis,” is among several articles in the April issue of Neurological Research that describe neurological infections in Latin America. Guest editor is Dr. Jaime Belmares, assistant professor in the Division of Infectious Diseases, Loyola University Chicago Stritch School of Medicine.

Neurocysticercosis is caused by a tapeworm found in pigs called Taenia solium. A person can get infected with the parasite by eating undercooked pork. That person then can excrete tapeworm eggs. The contamination spreads through food, water or surfaces contaminated with feces. A person can become infected, for example, by drinking contaminated water or putting contaminated fingers in the mouth.

Neurocysticercosis is most common in poor rural communities in developing countries with poor sanitation and hygiene and where pigs are allowed to roam freely and eat human feces.

Once inside the stomach, the tapeworm egg hatches, travels through the bloodstream and ends up in the muscles, brain or eyes. The worm, which can grow to more than one-half inch long, becomes enveloped in a fluid-filled cyst. Cysts in the muscles generally don’t cause symptoms. But cysts in the eyes can cause blurry vision, while cysts in the brain can cause headaches, encephalitis and seizures. Less common symptoms include confusion and difficulty with balance.

Seizures occur in up to 70 percent of patients. “They’re pretty dramatic,” Belmares said. “Every seizure needs to be properly evaluated.”

The article on neurocysticercosis was written by Dr. Adolfo Ramirez-Zamora, a former resident at Loyola now at the University of California at San Francisco and Tomas Alarcon, who did a rotation at Loyola during medical school.

Public release date: 15-Apr-2010

Health, life insurers hold $1.88 billion in fast-food stocks: AJPH article

Harvard researchers say insurers put profits over health

Just weeks after the passage of a health bill that will dramatically increase the number of Americans covered by private health insurers, Harvard researchers have detailed the extent to which life and health insurance companies are major investors in the fast-food industry – to the tune of nearly $2 billion.

Although fast food can be consumed responsibly, research has shown that fast-food consumption is linked to obesity and cardiovascular disease, two leading causes of death, and contributes to the poor health of children. The evidence is so compelling that as part of the new health law more than 200,000 fast-food and other chain restaurants will be required to include calorie counts on their menus, including their drive-through menus.

A new article on insurance company holdings, published online in today’s [Thursday, April 15] American Journal of Public Health, shows that U.S., Canadian and European-based insurance firms hold at least $1.88 billion of investments in fast-food companies.

“These data raise questions about the opening of vast new markets for private insurers at public expense, as is poised to happen throughout the United States as a result of the recent health care overhaul,” says lead author Dr. Arun Mohan.

Among the largest owners of fast-food stock are U.S.-based Prudential Financial, Northwestern Mutual and Massachusetts Mutual Life Insurance Company, and European-based ING.

U.S.-based Northwestern Mutual and Massachusetts Mutual Life Insurance Company both offer life insurance as well as disability and long-term care insurance. Northwestern Mutual owns $422.2 million of fast-food stock, with $318.1 million of McDonald’s. Mass Mutual owns $366.5 million of fast-food stock, including $267.2 in McDonald’s.

Holland-based ING, an investment firm that also offers life and disability insurance, has total fast-food holdings of $406.1 million, including $12.3 million in Jack in the Box, $311 million in McDonald’s, and $82.1 million in Yum! Brands (owner of Pizza Hut, KFC and Taco Bell) stock.

New Jersey-based Prudential Financial Inc. sells life insurance and long-term disability coverage. With total fast-food holdings of $355.5 million, Prudential Financial owns $197.2 of stock in McDonald’s and also has significant stakes in Burger King, Jack-in-the-Box, and Yum! Brands.

The researchers also itemize the fast-food holdings of London-based Prudential Plc, U.K.-based Standard Life, U.S.-based New York Life, Scotland-based Guardian Life, Canada-based Manulife and Canada-based Sun Life. (Table of data available at http://bit.ly/ds7elr ; all data current as of June 11, 2009.)

“Our data illustrate the extent to which the insurance industry seeks to turn a profit above all else,” says Dr. Wesley Boyd, senior author of the study. “Safeguarding people’s health and well-being take a back seat to making money.”

Mohan, Boyd and their co-authors, Drs. Danny McCormick, Steffie Woolhandler and David Himmelstein, all at the Cambridge Health Alliance and Harvard Medical School, culled their data from Icarus, a proprietary database of industrial, banking and insurance companies. Icarus draws upon Securities and Exchange Commission filings and news reports from providers like Dow Jones and Reuters. In addition, the authors obtained market capitalization data from Yahoo! Finance.

The authors write, “The health bill just enacted in Washington will likely expand the reach of the insurance industry. Canada and Britain are also considering further privatization of health insurance. Our article highlights the tension between profit maximization and the public good these countries face in expanding the role of private health insurers. If insurers are to play a greater part in the health care delivery system they ought to be held to a higher standard of corporate responsibility.”

Several of these same researchers, all of whom are affiliated with Physicians for a National Health Program, have previously published data about the extent to which the insurance industry is invested in tobacco. They say that because private, for-profit insurers have repeatedly put their own financial gain over the public’s health, readers in the United States, Canada and Europe should be wary about insurance firms’ participation in care.

Public release date: 15-Apr-2010

Diet high in B-vitamins lowers heart risks in Japanese study

In a large study in Japan, women who reported eating more foods containing the B-vitamins folate and B-6 were less likely to die from stroke and heart disease.

Japanese men reporting diets high in these B vitamins were less likely to die of heart failure.

DALLAS, April 15, 2010 — Eating more foods containing the B-vitamins folate and B-6 lowers the risk of death from stroke and heart disease for women and may reduce the risk of heart failure in men, according to Japanese research reported in Stroke: Journal of the American Heart Association.

“Japanese people need more dietary intake of folate and vitamin B-6, which may lead to the prevention of heart disease,” said Hiroyasu Iso, M.D., professor of public health at Osaka University.

The findings on the value of B vitamins were consistent with studies in Europe and North America, although the dietary consumption of vitamin B-6 is generally lower in Japan than in the United States.

Researchers analyzed data from 23,119 men and 35,611 women (ages 40–79) who completed food frequency questionnaires as part of the large Japan Collaborative Cohort (JACC) Study. During a median 14 years of follow-up, 986 died from stroke, 424 from heart disease and 2,087 from all diseases related to the cardiovascular system.

Investigators divided participants into five groups based on their intake of folate, vitamin B-6 and vitamin B-12. Comparing those with the diets lowest and highest for each nutrient, they found that higher consumption of folate and vitamin B-6 was associated with significantly fewer deaths from heart failure in men, and significantly fewer deaths from stroke, heart disease and total cardiovascular diseases in women. Vitamin B-12 intake was not associated with reduced mortality risk.

The protective effects of folate and vitamin B-6 didn’t change when researchers adjusted for the presence of cardiovascular risk factors, nor when they eliminated supplement users from the analysis.

Folate and vitamin B-6 may help guard against cardiovascular disease by lowering homocysteine levels, the investigators said. Homocysteine is an amino acid in the blood that’s affected by diet and heredity. Folic acid and other B vitamins help break down homocysteine in the body.

A direct causal link hasn’t been established, but evidence has shown that too much homocysteine may damage the inner lining of arteries and promote the formation of blood clots.

Sources of folate include vegetables and fruits, whole or enriched grains, fortified cereals, beans and legumes. Sources of vitamin B-6 include vegetables, fish, liver, meats, whole grains and fortified cereals.

Co-authors include: Renzhe Cui, M.D.; Chigusa Date, M.D.; Shogo Kikuchi, M.D.; Akiko Tamakoshi, M.D.; and the JACC study group. Author disclosures and funding sources are on the manuscript.

Public release date: 15-Apr-2010

Study shows potential benefit of dark chocolate for liver disease patients

Vienna, Austria, Thursday 15 April: Doctors could soon be prescribing a dose of dark chocolate to help patients suffering from liver cirrhosis and from dangerously high blood pressure in their abdomen, according to new research presented today at the International Liver CongressTM 2010, the Annual Meeting of the European Association for the Study of Liver in Vienna, Austria.

According to the Spanish research, eating dark chocolate reduces damage to the blood vessels of cirrhotic patients and also lowers blood pressure in the liver. Dark chocolate contains potent anti-oxidants which reduce the post-prandial (after-meal) blood pressure in the liver (or portal hypertension) associated with damaged liver blood vessels (endothelial dysfunction). The data also showed that eating dark chocolate may exert additional beneficial effects throughout the whole body. In comparison, white chocolate, which contains no beneficial ‘phytochemicals’, did not result in the same effects.

Professor Mark Thursz, MD FRCP, Vice Secretary of EASL and Professor of Hepatology, at Imperial College London said: “As well as advanced technologies and high science, it is important to explore the potential of alternative sources which can contribute to the overall wellbeing of a patient. This study shows a clear association between eating dark chocolate and portal hypertension and demonstrates the potential importance of improvements in the management of cirrhotic patients, to minimise the onset and impact of end stage liver disease and its associated mortality risks”.

Cirrhosis is scarring of the liver as a result of long-term, continuous damage to the liver . In cirrhosis, circulation in the liver is damaged by oxidative stress and reduced antioxidant systems. After eating, blood pressure in the abdominal veins usually increases due to increased blood flow to the liver.

This is particularly dangerous and damaging to cirrhotic patients as they already have increased blood pressure in the liver (portal hypertension) and elsewhere which, if severe, can cause blood vessel rupture. Thus, eating dark chocolate may ultimately prevent this potential threat to cirrhotic patients.

In this study 21 cirrhotic patients with end stage liver disease (child score 6.9±1.8;MELD 11±4; hepatic venous pressure gradient (HPVG*)16.6±3.8mmHg) were randomised to receive a standard liquid meal. Ten patients received the liquid meal containing dark chocolate (containing 85% cocoa, 0.55g of dark chocolate/Kg of body weight) while 11 patients received the liquid meal containing white chocolate which is devoid of cocoa flavonoids (anti-oxidant properties) according to body weight. HVPG, arterial pressure and portal blood flow (PBF)** were measured at baseline and 30 minutes after meal administration, using a US-Doppler.

Both meals caused a highly significant but similar increase in portal blood flow with a +24% increase in dark chocolate compared to +34% in those patients who received white chocolate. Interestingly, post-prandial hyperaemia*** was accompanied by an increase in HVPG resulting in a statistically significant increase (17.3±3.6mmHg to 19.1±2.6mmHg, p=0.07) for those patients eating dark chocolate and those receiving white chocolate (16.0±4.7mmHg to 19.7±4.1mmHg, p=0.003). Post-prandial increase in HVPG was markedly reduced in patients receiving dark chocolate (+10.3±16.3% Vs +26.3±12.7%, p=0.02).

###

*HVPG is blood pressure in the liver

**PBF refers to blood flow in the liver

***Hyperaemia refers to increase blood flow to tissues

Public release date: 15-Apr-2010

Low vitamin D levels associated with more asthma symptoms and medication use

Low levels of vitamin D are associated with lower lung function and greater medication use in children with asthma, according to researchers at National Jewish Health. In a paper published online this week in the Journal of Allergy & Clinical Immunology, Daniel Searing, MD, and his colleagues also reported that vitamin D enhances the activity of corticosteroids, the most effective controller medication for asthma.

“Asthmatic children in our study who had low levels of vitamin D were more allergic, had poorer lung function and used more medications,” said Dr. Searing. “Conversely, our findings suggest that vitamin D supplementation may help reverse steroid resistance in asthmatic children and reduce the effective dose of steroids needed for our patients.”

The researchers examined electronic medical records of 100 pediatric asthma patients referred to National Jewish Health. Overall, 47 percent of them had vitamin D levels considered insufficient, below 30 nanograms per milliliter of blood (ng/mL). Seventeen percent of the patients had levels below 20 ng/mL, which is considered deficient. These levels were similar to vitamin D levels found in the general population.

Patients low in vitamin D generally had higher levels of IgE, a marker of allergy, and responded positively to more allergens in a skin prick test. Allergies to the specific indoor allergens, dog and house dust mite, were higher in patients with low vitamin D levels. Low vitamin D also correlated with low FEV1, the amount of air a person can exhale in one second, and lower FEV1/FVC, another measure of lung function. Use of inhaled steroids, oral steroids and long-acting beta agonists were all higher in patients low in vitamin D.

“Our findings suggest two possible explanations,” said senior author Donald Leung, MD, PhD. “It could be that lower vitamin D levels contribute to increasing asthma severity, which requires more corticosteroid therapy. Or, it may be that vitamin D directly affects steroid activity, and that low levels of vitamin D make the steroids less effective, thus requiring more medication for the same effect.”

The researchers performed a series of laboratory experiments that indicated vitamin D enhances the action of corticosteroids. They cultured some immune cells with the corticosteroid dexamethasone alone and others with vitamin D first, then dexamethasone. The vitamin D significantly increased the effectiveness of dexamethasone. In one experiment vitamin D and dexamethasone together were more effective than 10 times as much dexamethasone alone.

The researchers also incubated immune-system cells for 72 hours with a staphylococcal toxin to induce corticosteroid resistance. Vitamin D restored the activity of dexamethasone.

“Our work suggests that vitamin D enhances the anti-inflammatory function of corticosteroids,’ said Dr. Leung. “If future studies confirm these findings vitamin D may help asthma patients achieve better control of their respiratory symptoms with less medication.”

Public release date: 16-Apr-2010

First evidence that chitosan could repair spinal damage

Chitosan offers hope for spinal injury patients

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Richard Borgens and his colleagues from the Center for Paralysis Research at the Purdue School of Veterinary Medicine have a strong record of inventing therapies for treating nerve damage. From Ampyra, which improves walking in multiple sclerosis patients to a spinal cord simulator for spinal injury victims, Borgens has had a hand in developing therapies that directly impact patients and their quality of life. Another therapy that is currently undergoing testing is the use of polyethylene glycol (PEG) to seal and repair damaged spinal cord nerve cells. By repairing the damaged membranes of nerve cells, Borgens and his team can restore the spinal cord’s ability to transmit signals to the brain. However, there is one possible clinical drawback: PEG’s breakdown products are potentially toxic. Is there a biodegradable non-toxic compound that is equally effective at targeting and repairing damaged nerve membranes? Borgens teamed up with physiologist Riyi Shi and chemist Youngnam Cho, who pointed out that some sugars are capable of targeting damaged membranes. Could they find a sugar that restored spinal cord activity as effectively as PEG? Borgens and his team publish their discovery that chitosan can repair damaged nerve cell membranes in The Journal of Experimental Biology on 16 April 2010 at http://jeb.biologists.org.

Having initially tested mannose and found that it did not repair spinal cord nerve membranes, Cho decided to test a modified form of chitin, one of the most common sugars that is found in crustacean shells. Converting chitin into chitosan, Cho isolated a segment of guinea pig spinal cord, compressed a section, applied the modified chitin and then added a fluorescent dye that could only enter the cells through damaged membranes. If the chitosan repaired the crushed membranes then the spinal cord tissue would be unstained, but if the chitosan had failed, the spinal cord neurons would be flooded with the fluorescent dye. Viewing a section of the spinal cord under the microscope, Cho was amazed to see that the spinal cord was completely dark. None of the dye had entered the nerve cells. Chitosan had repaired the damaged cell membranes.

Next Cho tested whether a dose of chitosan could prevent large molecules from leaking from damaged spinal cord cells. Testing for the presence of the colossal enzyme lactate dehydrogenase (LDH), Borgens admits he was amazed to see that levels of LDH leakage from chitosan treated spinal cord were lower than from undamaged spinal cords. Not only had the sugar repaired membranes at the compression site but also at other sites where the cell membranes were broken due to handling. And when the duo tested for the presence of harmful reactive oxygen species (ROS), released when ATP generating mitochondria are damaged, they found that ROS levels also fell after applying chitosan to the damaged tissue: chitosan probably repairs mitochondrial membranes as well as the nerve cell membranes.

But could chitosan restore the spinal cord’s ability to transmit electrical signals to the brain through a damaged region? Measuring the brain’s response to nerve signals generated in a guinea pig’s hind leg, the duo saw that the signals were unable to reach the brain through a damaged spinal cord. However, 30·min after injecting chitosan into the rodents, the signals miraculously returned to the animals’ brains. Chitosan was able to repair the damaged spinal cord so that it could carry signals from the animal’s body to its brain.

Borgens is extremely excited by this discovery that chitosan is able to locate and repair damaged spinal cord tissue and is even more enthusiastic by the prospect that nanoparticles of chitosan could also target delivery of neuroprotective drugs directly to the site of injury ‘giving us a dual bang for our buck,’ says Borgens.

Public release date: 18-Apr-2010

Vitamin and calcium supplements may reduce breast cancer risk

WASHINGTON, D.C. — Vitamins and calcium supplements appear to reduce the risk of breast cancer, according to findings presented at the American Association for Cancer Research 101st Annual Meeting 2010.

“It is not an immediate effect. You don’t take a vitamin today and your breast cancer risk is reduced tomorrow,” said Jaime Matta, Ph.D., professor in the Ponce School of Medicine in Puerto Rico. “However, we did see a long-term effect in terms of breast cancer reduction.”

Matta said the findings suggest that the calcium supplements are acting to enhance DNA repair capacity, a complex biological process involving more than 200 proteins that, if disrupted, can lead to cancer.

“This process involves at least five separate pathways and is critical for maintaining genomic stability,” said Matta. “When the DNA is not repaired, it leads to mutation that leads to cancer.”

The study included 268 women with breast cancer and 457 healthy controls. Women were more likely to have breast cancer if they were older, had a family history of breast cancer, had no history of breastfeeding and had lower DNA repair capacity.

Vitamin supplements appeared to reduce the risk of breast cancer by about 30 percent. Calcium supplements reduced the risk of breast cancer by 40 percent. After controlling for the level of DNA repair capacity, calcium supplements were no longer as protective, but the link between vitamin supplements and breast cancer reduction remained.

“We’re not talking about mega doses of these vitamins and calcium supplements, so this is definitely one way to reduce risk,” said Matta.

Public release date: 19-Apr-2010

Meat, especially if it’s well done, may increase risk of bladder cancer

Genetic variants in metabolism pathway further raise likelihood

WASHINGTON, D.C. – People who eat meat frequently, especially meat that is well done or cooked at high temperatures, may have a higher chance of developing bladder cancer, according to a large study at The University of Texas M. D. Anderson Cancer Center presented at the American Association for Cancer Research 101st Annual Meeting 2010. This risk appears to increase in people with certain genetic variants.

“It’s well known that meat cooked at high temperatures generates heterocyclic amines (HCAs) that can cause cancer,” said study presenter Jie Lin, Ph.D., assistant professor in M. D. Anderson’s Department of Epidemiology. “We wanted to find out if meat consumption increases the risk of developing bladder cancer and how genetic differences may play a part.”

Meat-eating habits examined

According to the American Cancer Society, almost 71,000 new cases of bladder cancer were diagnosed in this country last year, and more than 14,000 people died because of the disease. Men are at much higher risk of developing bladder cancer than women.

HCAs form when muscle meats, such as beef, pork, poultry or fish, are cooked at high temperatures. They are products of interaction between amino acids, which are the foundation of proteins, and the chemical creatine, which is stored in muscles. Past research has identified 17 HCAs that may contribute to cancer.

This study, which took place over 12 years, included 884 M. D. Anderson patients with bladder cancer and 878 people who did not have cancer. They were matched by age, gender and ethnicity.

Using a standardized questionnaire designed by the National Cancer Institute (NCI), researchers gathered information about each participant’s dietary habits. They then categorized people into four levels, ranging from lowest to highest red meat intake.

Well-done red meat nourishes cancer risk

The group with the highest red-meat consumption had almost one-and-a-half times the risk of developing bladder cancer as those who ate little red meat.

Specifically, consumption of beef steaks, pork chops and bacon raised bladder cancer risk significantly. Even chicken and fish – when fried – significantly raised the odds of cancer.

The level of doneness of the meat also had a marked impact. People whose diets included well-done meats were almost twice as likely to develop bladder cancer as those who preferred meats rare.

Further questioning of a subset of 177 people with bladder cancer and 306 people without bladder cancer showed that people with the highest estimated intake of three specific HCAs were more than two-and-a-half times more likely to develop bladder cancer than those with low estimated HCA intake.

“To quantify intakes of HCAs, we began three or four years ago to gather information on meat-cooking methods and doneness level, and then used a program developed by the NCI to estimate intakes of three major HCAs,” Lin said. “These data gave important information about the relationship between HCAs and bladder cancer.”

Genetic variants increase incidence

To take the investigation a step further, researchers analyzed each participant’s DNA to find if it contained genetic variants in the HCA metabolism pathways that may interact with red meat intake to increase the risk of cancer.

People with seven or more unfavorable genotypes as well as high red-meat intake were at almost five times the risk of bladder cancer.

“This research reinforces the relationship between diet and cancer,” said Xifeng Wu, M.D., Ph.D., professor in M. D. Anderson’s Department of Epidemiology and lead author on the study. “These results strongly support what we suspected: people, who eat a lot of red meat, particularly well-done red meat, such as fried or barbecued, seem to have a higher likelihood of bladder cancer. This effect is compounded if they carry high unfavorable genotypes in the HCA-metabolism pathway.”

Wu said this research is a step toward a future in which a comprehensive cancer-risk prediction model will integrate environmental, diet and genetic risk factors to predict an individual’s chances of developing cancer.

Public release date: 19-Apr-2010

Substance in breast milk kills cancer cells

A substance found in breast milk can kill cancer cells, reveal studies carried out by researchers at Lund University and the University of Gothenburg, Sweden.

Although the special substance, known as HAMLET (Human Alpha-lactalbumin Made LEthal to Tumour cells), was discovered in breast milk several years ago, it is only now that it has been possible to test it on humans. Patients with cancer of the bladder who were treated with the substance excreted dead cancer cells in their urine after each treatment, which has given rise to hopes that it can be developed into medication for cancer care in the future.

Discovered by chance

HAMLET was discovered by chance when researchers were studying the antibacterial properties of breast milk. Further studies showed that HAMLET comprises a protein and a fatty acid that are both found naturally in breast milk. So far, however, it has not been proven that the HAMLET complex is spontaneously formed in the milk. It is speculated, however, that HAMLET can form in the acidic environment of the babies´ stomachs. Laboratory experiments have shown that HAMLET kills 40 different types of cancer, and the researchers are now going on to study its effect on skin cancer, tumours in the mucous membranes and brain tumours. Importantly, HAMLET kills only cancer cells and does not affect healthy cells.

Public release date: 19-Apr-2010

Are doctors missing depression medication side effects?

Study finds patients report 20 times more side effects than recorded in charts

PROVIDENCE, RI – A study from Rhode Island Hospital shows that patients report side effects from medication for the treatment of depression 20 times more than psychiatrists have recorded in the charts. The researchers recommend the use of a self-administered patient questionnaire in clinical practice to improve the recognition of side effects for patients in treatment. The study is published in the Journal of Clinical Psychiatry, Volume 71, No. 4, now available online ahead of print.

One of the most frequent reasons for the discontinuation of medication to treat depression is the side effects that patients may experience. The premature discontinuation of medication is also associated with poorer treatment outcomes. In his recent study, lead researcher Mark Zimmerman, MD, director of outpatient psychiatry at Rhode Island Hospital, notes that despite the clinical importance of detecting side effects, few studies have examined the adequacy of the detection and documentation methods currently in use among clinicians.

Zimmerman and his colleagues asked 300 patients in ongoing treatment for depression to complete a self-administered version of the Toronto Side Effects Scale (TSES). The patients rated the frequency of the 31 side effects and the degree of trouble they experienced. Those patients’ charts were then examined to extract side effects information recorded by the treating psychiatrist.

The findings indicate that the mean number of side effects reported by the patients on the TSES was 20 times higher than the number recorded by the psychiatrist. When the self-reported side effects were limited to “frequently occurring” or “very bothersome” the rate was still found to be two to three times higher than recorded in their charts.

Zimmerman, who is also an associate professor of psychiatry and human behavior at The Warren Alpert Medical School of Brown University, says, “Despite the importance that side effects have on premature medication discontinuation, there is some evidence that clinicians may not do a thorough job of eliciting information regarding their presence. This study finds that clinicians do not record in their progress notes most side effects reported on a side effects questionnaire..”

While there may be several explanations for this, Zimmerman says, “Our research found that the only specific side effect that was regularly inquired about by clinicians was on sexual dysfunction, presumably because of concerns that some patients may be too embarrassed to spontaneously report that without prompting.” The researchers also suggest that patients stop reporting to psychiatrists the side effects that they have grown accustomed to, but patients reported these side effects in the self-report scale because there were specific questions about them. .

The researchers also question whether side effect frequencies reported in industry-sponsored studies may underestimate the prevalence of side effects from medication. As a result, clinicians may not be accurately informing patients of the potential likelihood of such side effects, and that lack of adequate preparation may result in patients prematurely discontinuing their medication.

Zimmerman says, “As a result of this study, we believe that ongoing dialogue about side effects during treatment will help to reduce premature medication discontinuation and would help reduce depression relapse rates. Incorporating a self-report questionnaire like the TSES may be helpful to adopt into clinical practice for the treatment of depression.”

Public release date: 19-Apr-2010

Vitamin K May Protect Against Developing Non-Hodgkin Lymphoma, Say Mayo Clinic Researchers

WASHINGTON — In the first study of vitamin K and Non-Hodgkin lymphoma risk, researchers at the Mayo Clinic campus in Minnesota have found that people who have higher intakes of vitamin K from their diet have a lower risk of developing Non-Hodgkin lymphoma. Non-Hodgkin Lymphoma is a cancer of the immune system and is the most common hematologic malignancy in the United States.

At the 101st Annual Meeting of the American Association for Cancer Research (AACR), the researchers report that the risk of developing Non-Hodgkin lymphoma was approximately 45 percent lower for participants who had vitamin K intakes in the top quartile of intake in the study (>108 ug/day), compared to participants who had intakes in the bottom quartile (<39 ug/day). This association remained after accounting for other factors such as age, sex, education, obesity, smoking, alcohol use and intake of foods with high amounts of antioxidants.

Vitamin K is a fat-soluble vitamin and is derived from either plants (phylloquinone or vitamin K1) or bacterial synthesis. This study estimated intake of the plant form of vitamin K from diet and supplement use. The most common sources of vitamin K1 in the diet include leaf lettuce and spinach, with smaller amounts found in other vegetables, vegetable oils and some fruits.

Researchers at the Mayo Comprehensive Cancer Center are studying the connection between diet and Non-Hodgkin lymphoma risk, and they became interested in a potential role for vitamin K. While vitamin K is best known for its essential function in several proteins involved in blood clotting (the name of the vitamin is derived from the German word “Koagulations”), it also appears to be important in other biological processes, including inhibition of inflammatory cytokines thought to play a role in Non-Hodgkin lymphoma, as well as pathways involved in cell cycle arrest and cell death.

“These results are provocative, since they are the first work we have done on the connection between vitamin K and Non-Hodgkin lymphoma, and this is a fairly strong protective effect,” says the study’s lead investigator, James Cerhan, M.D., Ph.D., a cancer epidemiologist. “However, as with all new findings, this will need to be replicated in other studies.”

The Mayo study enrolled 603 patients who were newly diagnosed with Non-Hodgkin lymphoma as well as 1,007 matched cancer-free “control” participants. Researchers asked the participants to answer a food questionnaire about their usual intake of over 120 food items two years prior to their cancer diagnosis or enrollment into the study (controls). They also asked about use of a variety of supplements. Vitamin K intake was estimated from this data.

While there was a clear trend showing that a greater intake of vitamin K from dietary sources was associated with a lower risk of Non-Hodgkin lymphoma, the use of vitamin K supplements presented a slightly different picture. Increasing intake of vitamin K from supplements did protect against Non-Hodgkin lymphoma, but reached a point where the highest intake offered no reduction in risk. “The significance of this finding is unclear,” notes Dr. Cerhan, “but suggests that taking high doses of supplements is unlikely to be helpful.” Dr. Cerhan also notes that people taking certain oral anticoagulants or seizure medications should closely follow their physician’s dietary recommendations with respect to vitamin K intake, since vitamin K can interfere with these drugs.

“Whether the protective effect we observed is due to vitamin K intake, or some other dietary or lifestyle exposure, cannot be definitely assessed in this study,” notes Dr. Cerhan. “But these findings add to a lot of other data that support a diet that includes plenty of green leafy vegetables in order to prevent many cancers as well as other diseases.”

The study was funded by the National Cancer Institute.

Public release date: 19-Apr-2010

Obesity gene, carried by more than a third of the U.S. population, leads to brain tissue loss

Three years ago, geneticists reported the startling discovery that nearly half of all people in the U.S. with European ancestry carry a variant of the fat mass and obesity associated (FTO) gene, which causes them to gain weight — from three to seven pounds, on average — but worse, puts them at risk for obesity.

Now, UCLA researchers have found that the same gene allele, which is also carried by roughly one-quarter of U.S. Hispanics, 15 percent of African Americans and 15 percent of Asian Americans, may have another deleterious effect.

Reporting in the early online edition of the journal Proceedings of the National Academy of Sciences, senior study author Paul Thompson, a UCLA professor of neurology; lead authors April Ho and Jason Stein, graduate students in Thompson’s lab; and colleagues found that the FTO variant is also associated with a loss of brain tissue. This puts more than a third of the U.S. population at risk for a variety of diseases, such as Alzheimer’s.

Using magnetic resonance imaging, the researchers generated three-dimensional “maps” of brain volume differences in 206 healthy elderly subjects drawn from 58 sites in the U.S. as part of the Alzheimer’s Disease Neuroimaging Initiative, a large, five-year study aimed at better understanding factors that help the brain resist disease as it ages.

They found that there was consistently less tissue in the brains of those who carry the FTO allele, compared with non-carriers. Individuals with the “bad” version of the FTO gene had an average of 8 percent less tissue in the frontal lobes, the “command center” of the brain, and 12 percent less in the occipital lobes, areas in the back of the brain responsible for vision and perception. Further, the brain differences could not be directly attributed to other obesity-related factors such as cholesterol levels, diabetes or high blood pressure.

Thompson called the findings worrying and mysterious.

“The results are curious. If you have the bad FTO gene, your weight affects your brain adversely in terms of tissue loss,” he said. “If you don’t carry FTO, higher body weight doesn’t translate into brain deficits; in fact, it has nothing to do with it. This is a very mysterious, widespread gene.”

People who carry this specific DNA sequence are heavier on average, and their waist circumference is half an inch bigger.

This is a large percentage of the population, said Thompson, who is also a member of UCLA’s Brain Research Institute and the UCLA Laboratory of Neuro Imaging.

“This is a shocking finding. Any loss of brain tissue puts you at greater risk for functional decline,” he said. “The risk gene divides the world into two camps ― those who have the FTO allele and those who don’t.”

But the news is not necessarily completely negative, Thompson said, because “carriers of the risk gene can exercise and eat healthily to resist both obesity and brain decline.”

Thompson sees both a public health message and a science message in this finding.

“Half of the world carries this dangerous gene. But a healthy lifestyle will counteract the risk of brain loss, whether you carry the gene or not. So it’s vital to boost your brain health by being physically active and eating a balanced diet,” he said.

And from a scientific standpoint, he said, “the gene discovery will help to develop and fine tune the anti-dementia drugs being developed to combat brain aging.”

Funding for the study came from the National Institutes of Health and from private industry. The authors report no conflict of interest.

________________________________

These reports are done with the appreciation of all the Doctors, Scientist, and other

Medical Researchers who sacrificed their time and effort. In order to give people the

ability to empower themselves. Without the base aspirations for fame, or fortune.

Just honorable people, doing honorable things.

Health Research Report

80th Issue 22 APR 2010

Compiled By Ralph Turchiano

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Alzheimer’s disease may protect against cancer and vice versa

2009 study posted for filing

Contact: Rachel Seroka rseroka@aan.com 651-695-2738 American Academy of Neurology

ST. PAUL, Minn. – People who have Alzheimer’s disease may be less likely to develop cancer, and people who have cancer may be less likely to develop Alzheimer’s disease, according to a new study published in the December 23, 2009, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Discovering the links between these two conditions may help us better understand both diseases and open up avenues for possible treatments,” said study author Catherine M. Roe, PhD, of Washington University School of Medicine in St. Louis, MO, and a member of the American Academy of Neurology.

For the study, researchers looked at a group of 3,020 people age 65 and older who were enrolled in the Cardiovascular Health Study and followed them for an average of five years to see whether they developed dementia and an average of eight years to see whether they developed cancer. At the start of the study, 164 people (5.4 percent) already had Alzheimer’s disease and 522 people (17.3 percent) already had a cancer diagnosis.

During the study, 478 people developed dementia and 376 people developed invasive cancer. For people who had Alzheimer’s disease at the start of the study, the risk of future cancer hospitalization was reduced by 69 percent compared to those who did not have Alzheimer’s disease when the study started. For Caucasian people who had cancer when the study started, their risk of developing Alzheimer’s disease was reduced by 43 percent compared to people who did not have cancer at the start of the study, although that finding was not evident in minority groups.

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The study was supported by the National Institutes of Health, the National Heart, Lung, and Blood Institute, the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, the National Center for Research Resources, and the Washington University Alzheimer’s Disease Research Center.

The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer’s disease, epilepsy, Parkinson’s disease, and multiple sclerosis.

For more information about the American Academy of Neurology, visit http://www.aan.com.

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73rd Health Research Report 05 JAN 2010 – Reconstruction

 

In this issue:

1. Growing evidence suggests progesterone should be considered a treatment option for traumatic brain injuries

2. Alzheimer’s disease may protect against cancer and vice versa

3. Citrus surprise: Vitamin C boosts the reprogramming of adult cells into stem cells

4. Chlorophylls effective against aflatoxin

5. New year, new vitamin C discovery: It ‘cures’ mice with accelerated aging disease

6. (glycyrrhizin extracted from licorice root) A trip to the candy store might help ward off rare, but deadly infections

7. Running shoes may cause damage to knees, hips and ankles

8. Natural compound ( Quercetin) blocks hepatitis C infection

9. Caffeine consumption associated with less severe liver fibrosis

 

Public release date: 22-Dec-2009

Growing evidence suggests progesterone should be considered a treatment option for traumatic brain injuries

Researchers at Emory University in Atlanta, GA, recommend that progesterone (PROG), a naturally occurring hormone found in both males and females that can protect damaged cells in the central and peripheral nervous systems, be considered a viable treatment option for traumatic brain injuries, according to a clinical perspective published in the January issue of the American Journal of Roentgenology.

“Traumatic brain injury (TBI) is an important clinical problem in the United States and around the world,” said Donald G. Stein, PhD, lead author of the paper. “TBI has received more attention recently because of its high incidence among combat casualties in Iraq and Afghanistan. Current Department of Defense statistics indicated that as many as 30 percent of wounded soldiers seen at Walter Reed Army Hospital have suffered a TBI, a finding that has stimulated government interest in developing a safe and effective treatment for this complex disorder,” said Stein.

“Growing evidence indicates that post-injury administration of PROG in a variety of brain damage models can have beneficial effects, leading to substantial and sustained improvements in brain functionality. PROG given to both males and females can cross the blood-brain barrier and reduce edema (swelling) levels after TBI; in different models of cerebral ischemia (restriction of blood supply), significantly reduce the area of necrotic cell death and improve behavioral outcomes; and protect neurons distal to the injury that would normally die,” said Stein.

PROG was recently tested in two phase 2 clinical trials for traumatic brain injury and will begin a phase 3 NIH sponsored trial soon.

“Given its relatively high safety profile, its ease of administration, its low cost and ready availability, PROG should be considered a viable treatment option — especially because, in brain injury, so little else is currently available,” said Stein.

 

Public release date: 23-Dec-2009

Alzheimer’s disease may protect against cancer and vice versa

Embargoed for release until 4 p.m. ET, Wednesday, Dec. 23, 2009

ST. PAUL, Minn. – People who have Alzheimer’s disease may be less likely to develop cancer, and people who have cancer may be less likely to develop Alzheimer’s disease, according to a new study published in the December 23, 2009, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Discovering the links between these two conditions may help us better understand both diseases and open up avenues for possible treatments,” said study author Catherine M. Roe, PhD, of Washington University School of Medicine in St. Louis, MO, and a member of the American Academy of Neurology.

For the study, researchers looked at a group of 3,020 people age 65 and older who were enrolled in the Cardiovascular Health Study and followed them for an average of five years to see whether they developed dementia and an average of eight years to see whether they developed cancer. At the start of the study, 164 people (5.4 percent) already had Alzheimer’s disease and 522 people (17.3 percent) already had a cancer diagnosis.

During the study, 478 people developed dementia and 376 people developed invasive cancer. For people who had Alzheimer’s disease at the start of the study, the risk of future cancer hospitalization was reduced by 69 percent compared to those who did not have Alzheimer’s disease when the study started. For Caucasian people who had cancer when the study started, their risk of developing Alzheimer’s disease was reduced by 43 percent compared to people who did not have cancer at the start of the study, although that finding was not evident in minority groups.

Public release date: 24-Dec-2009

Citrus surprise: Vitamin C boosts the reprogramming of adult cells into stem cells

Famous for its antioxidant properties and role in tissue repair, vitamin C is touted as beneficial for illnesses ranging from the common cold to cancer and perhaps even for slowing the aging process. Now, a study published online on December 24th by Cell Press in the journal Cell Stem Cell uncovers an unexpected new role for this natural compound: facilitating the generation of embryonic-like stem cells from adult cells.

Over the past few years, we have learned that adult cells can be reprogrammed into cells with characteristics similar to embryonic stem cells by turning on a select set of genes. Although the reprogrammed cells, called induced pluripotent stem cells (iPSCs), have tremendous potential for regenerative medicine, the conversion is extremely inefficient.

“The low efficiency of the reprogramming process has hampered progress with this technology and is indicative of how little we understand it. Further, this process is most challenging in human cells, raising a significant barrier for producing iPSCs and serious concerns about the quality of the cells that are generated,” explains senior study author Dr. Duanqing Pei from the South China Institute for Stem Cell Biology and Regenerative Medicine at the Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences.

Dr. Pei and colleagues measured the production of reactive oxygen species or ROS during reprogramming and discovered a potential link between high ROS and low reprogramming efficiency. They became particularly interested in antioxidants, hypothesizing that they might suppress ROS and cell senescence, which seems to be a major roadblock for the generation of iPSCs.

The researchers found that adding vitamin C, an essential nutrient that is abundant in citrus fruits, enhanced iPSC generation from both mouse and human cells. Vitamin C accelerated gene expression changes and promoted a more efficient transition to the fully reprogrammed state. Somewhat to their surprise, they found that other antioxidants do not have the same effect, but vitamin C does seem to act at least in part through slowing cell senescence.

“Our results highlight a simple way to improve iPSC generation and provide additional insight into the mechanistic basis of reprogramming,” concludes Dr. Pei. “It is also of interest that a vitamin with long-suspected anti-aging effects has such a potent influence on reprogramming, which can be considered a reversal of the aging process at the cellular level. It is likely that our work may stimulate further research in this area as well.”

 

Public release date: 29-Dec-2009

Chlorophylls effective against aflatoxin

CORVALLIS, Ore. – A new study has found that chlorophyll and its derivative chlorophyllin are effective in limiting the absorption of aflatoxin in humans. Aflatoxin is produced by a fungus that is a contaminant of grains including corn, peanuts and soybeans; it is known to cause liver cancer – and can work in concert with other health concerns, such as hepatitis.

Levels of aflatoxin are carefully regulated in the United States, but are often found in the food supplies of developing nations, especially those with poor storage facilities.

OSU scientist George Bailey, a distinguished professor of environmental and molecular toxicology, pioneered studies of aflatoxin in China, where he found that in one region, one out of every 10 adults died from liver cancer.

But what has the science world particularly intrigued with this follow-up study is the methodology used by the researchers – a new “Phase 0” approach that safely tests low levels of carcinogens in human volunteers to measure the total aflatoxin exposure and to determine the effect of dietary chlorophlls on reducing this exposure.

Results of the study were just published in the journal Cancer Prevention Research.

Bailey and several other researchers, including lead author Carole Jubert, were part of the recent study. The journal also included a perspective written by a pair of Johns Hopkins researchers – Thomas Kensler and John Groopman – who praise the methodology and suggest that these Phase 0 “microdosing” studies should be expanded.

They wrote: “…microdosing studies with carcinogens have the potential to provide important insights into chemopreventive interventions and to enhance the overall clinical development and safety evaluation of preventive agents.”

The Phase 0 study “…may open the door for all kinds of new research,” said Jubert, a former researcher in Bailey’s lab at OSU’s Linus Pauling Institute. Jubert now works for Life Microsystems, an OSU spinoff company that hopes to continue work with natural products grown in Oregon, including pure chlorophylls.

“The technology is not particularly difficult,” she added. “It’s just a novel approach to evaluate toxin exposure in humans.”

In their study, Jubert and her colleagues gave very low doses of aflatoxin labeled with carbon-14 isotopes as a tracer to four human volunteers. They then gave the volunteers the same doses of aflatoxin along with doses of either chlorophyll or chlorophyllin, which previously had been shown to reduce carcinogen bioavailability in trout and rats. Using an accelerator mass spectrometer, they measured the rate of aflaxtoxin bioavailability. This technique is extremely sensitive, the researchers say, allowing measurement of minute amounts of any labeled compound.

Their research revealed rapid absorption of aflatoxin, which was significantly limited after the chlorophyll and chlorophyllin treatments.

“The beauty of this kind of ‘Phase 0’ study is the use of ultra-sensitive technology and ‘microdoses’ of environmental carcinogens to study toxicokinetics within the human body,” said John Mata, an OSU pharmacologist and second author on the study. “These measurements can be important because they allow us to better design future studies to understand the effects of dietary constituents on cancer risk.

“In this case, clearly the results merit further study,” Mata added. “We showed that aflatoxin is absorbed quite rapidly and that chlorophyll and chlorophyllin have an ameliorating effect, preventing the toxin from getting into the bloodstream. Further studies can more precisely explore the interactions, as well as dosage levels.”

Jubert and Mata also have tested the feasibility of using similar technology on human exposure to other toxins, including smokers who ingest carcinogens through cigarette smoke.

Mata, a professor in OSU’s College of Veterinary Medicine, is a pharmacologist who previously worked in the drug industry. He said Phase 1 studies are designed to see if a compound is safe; Phase 2 expands the scope of the project, and Phase 3 looks at the compounds’ efficacy. Phase 0 represents a new concept – a way to measure the kinetics of a drug by using extremely small doses that pose little risk to the volunteers.

In this case, the amount of radiation given the human volunteers was equal to that you would encounter from a one-hour airplane ride; the level of aflatoxin administered was 1/30th the amount the Food and Drug Administration allows in a peanut butter sandwich.

Public release date: 4-Jan-2010

New year, new vitamin C discovery: It ‘cures’ mice with accelerated aging disease

New research in the FASEB Journal reports vitamin C reverses abnormalities caused by Werner syndrome gene, including cancer, obesity, diabetes, heart failure and high cholesterol

A new research discovery published in the January 2010 print issue of the FASEB Journal (http://www.fasebj.org) suggests that treatments for disorders that cause accelerated aging, particularly Werner’s syndrome, might come straight from the family medicine chest. In the research report, a team of Canadian scientists show that vitamin C stops and even reverses accelerated aging in a mouse model of Werner’s syndrome, but the discovery may also be applicable to other progeroid syndromes. People with Werner’s syndrome begin to show signs of accelerated aging in their 20s and develop age-related diseases and generally die before the age of 50.

“Our study clearly indicates that a healthy organism or individuals with no health problems do not require a large amount of vitamin C in order to increase their lifespan, especially if they have a balanced diet and they exercise,” said Michel Lebel, Ph.D., co-author of the study from the Centre de Recherche en Cancerologie in Quebec, Canada. “An organism or individual with a mutation in the WRN gene or any gene affected by the WRN protein, and thus predisposes them to several age-related diseases, may benefit from a diet with the appropriate amount of vitamin C.”

Scientists treated both normal mice and mice with a mutation in the gene responsible for Werner’s syndrome (WRN gene) with vitamin C in drinking water. Before treatment, the mice with a mutated WRN gene were fat, diabetic, and developing heart disease and cancer. After treatment, the mutant mice were as healthy as the normal mice and lived a normal lifespan. Vitamin C also improved how the mice stored and burned fat, decreased tissue inflammation and decreased oxidative stress in the WRN mice. The healthy mice did not appear to benefit from vitamin C.

“Vitamin C has become one of the most misunderstood substances in our medicine cabinets and food,” said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal. “This study and others like it help explain how and why this chemical can help to defend some, but certainly not all, people from premature senescence.”

Ralph’s note – “ The healthy mice did not appear to benefit from vitamin C” If the mice were healthy, What benefit were they looking for Specifically (I.e. Immortality, Laser Vision, etc..)

 

Public release date: 4-Jan-2010

(glycyrrhizin extracted from licorice root) A trip to the candy store might help ward off rare, but deadly infections

New research in the Journal of Leukocyte Biology shows that glycyrrhizin extracted from licorice root helps the body defend against Pseudomonas aeruginosa infection

As it turns out, children were not the only ones with visions of sugar plums dancing in their heads over this past holiday season. In a new research report published in the January 2010 issue of the Journal of Leukocyte Biology (http://www.jleukbio.org), a team of scientists from the University of Texas Medical Branch and Shriners Hospitals for Children show how a compound from licorice root (glycyrrhizin from Glycyrrhiza glabra) might be an effective tool in battling life-threatening, antibiotic-resistant infections resulting from severe burns. Specifically, they found that in burned mice, glycyrrhizin improved the ability of damaged skin to create small proteins that serve as the first line of defense against infection. These proteins, called antimicrobial peptides, work by puncturing the cell membranes of bacteria similar to how pins pop balloons.

“It is our hope that the medicinal uses of glycyrrhizin will lead to lower death rates associated with infection in burn patients,” said Fujio Suzuki, Ph.D., one of the researchers involved in the work. Suzuki also said that more research is necessary to determine if this finding would have any implications for people with cystic fibrosis, who can develop Pseudomonas aeruginosa infections in their lungs.

To make this discovery, Suzuki and colleagues used three groups of mice. The first group was normal, the second group was burned and untreated, and the third group was burned and treated with glycyrrhizin. The skin of the untreated burned mice did not have any detectable antimicrobial peptides that prevent bacteria from growing and spreading, but the normal mice did. The skin of the untreated burned mice also had immature myeloid cells, which indicate an inability of the skin to produce antimicrobial peptides needed to prevent infection. The mice treated with glycyrrhizin, however, were more like the normal mice as they had the antimicrobial peptides and no immature myeloid cells.

“Burns are the most painful of all injuries,” said John Wherry, Ph.D., Deputy Editor of the Journal of Leukocyte Biology, “and the deadly Pseudomonas infections that can result from severe burns do more than add insult to those injuries. This research should serve as an important stepping stone toward helping develop new drugs that help prevent or treat Pseudomonas.”

 

Public release date: 4-Jan-2010

Running shoes may cause damage to knees, hips and ankles

Greater stresses on joints than running barefoot or walking in high-heeled shoes observed

New York, NY, January 4, 2010 – Knee osteoarthritis (OA) accounts for more disability in the elderly than any other disease. Running, although it has proven cardiovascular and other health benefits, can increase stresses on the joints of the leg. In a study published in the December 2009 issue of PM&R: The journal of injury, function and rehabilitation, researchers compared the effects on knee, hip and ankle joint motions of running barefoot versus running in modern running shoes. They concluded that running shoes exerted more stress on these joints compared to running barefoot or walking in high-heeled shoes.

Sixty-eight healthy young adult runners (37 women), who run in typical, currently available running shoes, were selected from the general population. None had any history of musculoskeletal injury and each ran at least 15 miles per week. A running shoe, selected for its neutral classification and design characteristics typical of most running footwear, was provided to all runners. Using a treadmill and a motion analysis system, each subject was observed running barefoot and with shoes. Data were collected at each runner’s comfortable running pace after a warm-up period.

The researchers observed increased joint torques at the hip, knee and ankle with running shoes compared with running barefoot. Disproportionately large increases were observed in the hip internal rotation torque and in the knee flexion and knee varus torques. An average 54% increase in the hip internal rotation torque, a 36% increase in knee flexion torque, and a 38% increase in knee varus torque were measured when running in running shoes compared with barefoot.

These findings confirm that while the typical construction of modern-day running shoes provides good support and protection of the foot itself, one negative effect is the increased stress on each of the 3 lower extremity joints. These increases are likely caused in large part by an elevated heel and increased material under the medial arch, both characteristic of today’s running shoes.

Writing in the article, lead author D. Casey Kerrigan, MD, JKM Technologies LLC, Charlottesville, VA, and co-investigators state, “Remarkably, the effect of running shoes on knee joint torques during running (36%-38% increase) that the authors observed here is even greater than the effect that was reported earlier of high-heeled shoes during walking (20%-26% increase). Considering that lower extremity joint loading is of a significantly greater magnitude during running than is experienced during walking, the current findings indeed represent substantial biomechanical changes.” Dr. Kerrigan concludes, “Reducing joint torques with footwear completely to that of barefoot running, while providing meaningful footwear functions, especially compliance, should be the goal of new footwear designs.”

Public release date: 4-Jan-2010

Natural compound ( Quercetin) blocks hepatitis C infection

Finding may lead to a new treatment

Researchers have identified two cellular proteins that are important factors in hepatitis C virus infection, a finding that may result in the approval of new and less toxic treatments for the disease, which can lead to liver cancer and cirrhosis.

An estimated 270 to 300 million people worldwide are infected with hepatitis C and the conventional treatments – interferon and ribavirin – can have significant side effects. A new drug targeting cellular proteins rather than viral proteins would be a valuable addition to the treatment arsenal, said Samuel French, an assistant professor of pathology and senior author of the study.

French and his team set out to identify the cellular factors involved in hepatitis C replication and, using mass spectrometry, found that heat shock proteins (HSPs) 40 and 70 were important for viral infection. HSP 70 was previously known to be involved, but HSP 40 was linked for the first time to hepatitis C infection, French said. They further showed that the natural compound Quercetin, which inhibits the synthesis of these proteins, significantly inhibits viral infection in tissue culture.

“This is an important finding because we can block these proteins with the idea of reducing the level of the virus in people and, ideally, completely eliminate it,” said French, who also is a researcher at UCLA’s Jonsson Comprehensive Cancer Center.

The study appeared in the most recent issue of the journal Hepatology.

Since Quercetin has been shown to inhibit hepatitis C infection, French said, a Phase I clinical trial will be launched at UCLA to determine if the compound is safe and effective.

Quercetin is a plant-derived bioflavonoid, and is used by some people as a nutritional supplement. Laboratory studies show it may have anti-inflammatory and antioxidant properties, and it is being investigated for a wide range of potential health benefits. Currently, there are early-stage clinical trials testing quercetin for safety and efficacy against sarcoidosis, asthma and glucose absorption in obesity and diabetes.

“Because Quercetin targets cellular proteins rather than viral proteins, there is less likelihood of developing viral resistance,” French said. “Cellular proteins cannot change like viral proteins can.”

Many patients in the United States have a type of hepatitis C virus that does not respond to the standard treatments. In these cases, if the virus can’t be blocked, end-stage liver disease and, ultimately, death may occur. Once HSP 40 and 70 were identified, French and his team used Quercetin in an attempt to block the proteins and found that the compound “reduced infectious particle production at non-toxic concentrations,” according to the study.

“Quercetin may allow for the dissection of the viral life cycle and has potential therapeutic use to reduce virus production with low associated toxicity,” the study states.

The UCLA clinical trial will most likely target those with type 1 hepatitis C, which is the non-responsive type prevalent in this country. Only about 50 percent of those with type 1 hepatitis C respond to treatment, French said.

Volunteers with type 1 hepatitis C who opt not to undergo conventional therapies would be recruited for the study. In other studies in other diseases, Quercetin has resulted in no significant side effects, French said.

“A non-toxic treatment for chronic hepatitis C would be great because our current therapies have significant side effects and only a certain percentage of the patient population responds,” French said.

Public release date: 5-Jan-2010

Natural compounds in pomegranates may prevent growth of hormone-dependent breast cancer

Eating fruit, such as pomegranates, that contain anti-aromatase phytochemicals reduces the incidence of hormone-dependent breast cancer, according to results of a study published in the January issue of Cancer Prevention Research, a journal of the American Association for Cancer Research.

Pomegranate is enriched in a series of compounds known as ellagitannins that, as shown in this study, appear to be responsible for the anti-proliferative effect of the pomegranate.

“Phytochemicals suppress estrogen production that prevents the proliferation of breast cancer cells and the growth of estrogen-responsive tumors,” said principal investigator Shiuan Chen, Ph.D., director of the Division of Tumor Cell Biology and co-leader of the Breast Cancer Research Program at City of Hope in Duarte, Calif.

Previous research has shown that pomegranate juice — punica granatum L — is high in antioxidant activity, which is generally attributed to the fruit’s high polyphenol content. Ellagic acid found in pomegranates inhibits aromatase, an enzyme that converts androgen to estrogen. Aromatase plays a key role in breast carcinogenesis; therefore, the growth of breast cancer is inhibited.

Chen, along with Lynn Adams, Ph.D., a research fellow at Beckman Research Institute of City of Hope, and colleagues, evaluated whether phytochemicals in pomegranates can suppress aromatase and ultimately inhibit cancer growth.

After screening and examining a panel of 10 ellagitannin-derived compounds in pomegranates, the investigators found that those compounds have the potential to prevent estrogen-responsive breast cancers. Urolithin B, which is a metabolite produced from ellagic acid and related compounds, significantly inhibited cell growth.

“We were surprised by our findings,” said Chen. “We previously found other fruits, such as grapes, to be capable of the inhibition of aromatase. But, phytochemicals in pomegranates and in grapes are different.”

According to Gary Stoner, Ph.D., professor in the Department of Internal Medicine at Ohio State University, additional studies will be needed to confirm the chemopreventive action of Urolithin B against hormone-dependent breast cancer.

“This is an in vitro study in which relatively high levels of ellagitannin compounds were required to demonstrate an anti-proliferative effect on cultured breast cancer cells,” said Stoner, who is not associated with this study. “It’s not clear that these levels could be achieved in animals or in humans because the ellagitannins are not well absorbed into blood when provided in the diet.”

Stoner believes these results are promising enough to suggest that more experiments with pomegranate in animals and humans are warranted.

Powel Brown, M.D., Ph.D., medical oncologist and chairman of the Clinical Cancer Prevention Department at the University of Texas M. D. Anderson Cancer Center, agreed with Stoner’s sentiments and said these results are intriguing. He recommended that future studies focus on testing pomegranate juice for its effect on estrogen levels, menopausal symptoms, breast density or even as a cancer preventive agent.

“More research on the individual components and the combination of chemicals is needed to understand the potential risks and benefits of using pomegranate juice or isolated compounds for a health benefit or for cancer prevention,” Brown said. “This study does suggest that studies of the ellagitannins from pomegranates should be continued.”

Until then, Stoner said people “might consider consuming more pomegranates to protect against cancer development in the breast and perhaps in other tissues and organs.”

Public release date: 5-Jan-2010

Caffeine consumption associated with less severe liver fibrosis

Study finds caffeine in sources other than coffee does not have similar effect

Researchers from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) determined that patients with chronic hepatitis C virus (HCV) who consumed more than 308 mg of caffeine daily had milder liver fibrosis. The daily amount of caffeine intake found to be beneficial is equivalent to 2.25 cups of regular coffee. Other sources of caffeine beyond coffee did not have the same therapeutic effect. Details of this study are available in the January 2010 issue of Hepatology, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases.

Liver fibrosis or scaring of the liver is the second stage of liver disease and characterized by a degradation of liver function due to accumulated connective tissue. Past studies have looked at modifiable behaviors, such as coffee consumption, that mitigate the progression of liver disease. A number of studies have looked at the benefits of higher coffee intake with results that include: lower prevalence of chronic liver disease, reduced risk of hepatocellular carcinoma (liver cancer), and lower risk of death from cirrhosis complications. “From data collected to date it remains unclear whether coffee itself, or caffeine provides the beneficial effect,” said Apurva Modi, M.D. and lead author of the current study that focuses on caffeine intake and its impact on liver fibrosis.

From January 2006 to November 2008 all patients evaluated in the Liver Disease Branch of the National Institutes of Health were asked to complete a questionnaire to determine caffeine consumption. Questions were asked pertaining to all sources of caffeine including regular and diet soft drinks; regular and decaffeinated coffee; black, green, Chinese and herbal teas; cocoa and hot chocolate; caffeine-fortified drinks; chocolate candy; caffeine pills; and medications with caffeine. Participants were asked about their frequency of caffeine consumption, which was quantified as never; 1-3 times per month; 1, 2-4, or 5-6 times per week; 1, 2-3, 4-5, and 6 or more times per day.

The analysis included 177 participants who were undergoing liver biopsy with a mean age of 51 years and mean body mass index (BMI) of 27.5. Of those in the cohort 56% were male, 59% Caucasian, 19% Black, 19% Asian, 3% Hispanic, and 68% had chronic HCV. Daily consumption of caffeine from food and beverages raged from none to 1028 mg/day with an average of 195 mg/day, which is equivalent to 1.4 cups of coffee daily. Most caffeine consumed came from regular coffee (71%) followed by caffeinated soda (13%), and black tea (4%). Repeated administration of the questionnaire within a 6-month period displayed consistent responses suggesting caffeine intake does not significantly change over time.

Patients with an Ishak fibrosis score of less than 3 had a mean caffeine intake of 212 mg/day compared with 154 mg/day for those with more advanced fibrosis. The Ishak fibrosis score is the preferred system that measures degree of liver scarring with 0 representing no fibrosis through 6 indicating cirrhosis. For each 67 mg increase in caffeine consumption (about one half cup of coffee) there was a 14% decrease in the odds of advanced fibrosis for patients with HCV. “Our data suggest that a beneficial effect requires caffeine consumption above a threshold of approximately 2 coffee-cup equivalents daily,” noted Dr. Modi. The protective effects of consuming more than 308 mg of caffeine daily persisted after controlling for age, sex, race, liver disease, BMI and alcohol intake for all study participants.

Researchers further evaluated caffeine and coffee separately to determine the individual effect of each on fibrosis. Results showed that consumption of caffeinated soda, green or black tea was not associated with reduced liver fibrosis. However, a significant protective effect could have been missed due to small numbers, as 71% of total caffeine consumed came from coffee. Caffeinated coffee had the most pronounced effect on reduced liver fibrosis. The authors suggest that further research is needed to determine if the protective benefits of coffee/caffeine intake plateau at amounts beyond the daily consumption threshold.

________________________________

 

These reports are done with the appreciation of all the Doctors, Scientist, and other

Medical Researchers who sacrificed their time and effort. In order to give people the

ability to empower themselves. Without the base aspirations for fame, or fortune.

Just honorable people, doing honorable things.

Health Research Report

73rd  Issue 05 JAN 2010

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/engineeringevil

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Green tea chemical combined with another may hold promise for treatment of brain disorders: EGCG, can prevent and destroy a variety of protein structures known as amyloids

2009 study posted for filing

Contact: patti Jacobs pjacobs12@comcast.net 617-864-2712 Boston Biomedical Research Institute

Watertown, MA—Scientists at Boston Biomedical Research Institute (BBRI) and the University of Pennsylvania have found that combining two chemicals, one of which is the green tea component EGCG, can prevent and destroy a variety of protein structures known as amyloids. Amyloids are the primary culprits in fatal brain disorders such as Alzheimer’s, Huntington’s, and Parkinson’s diseases. Their study, published in the current issue of Nature Chemical Biology (December 2009), may ultimately contribute to future therapies for these diseases.

“These findings are significant because it is the first time a combination of specific chemicals has successfully destroyed diverse forms of amyloids at the same time,” says Dr. Martin Duennwald of BBRI, who co-led the study with Dr. James Shorter of University of Pennsylvania School of Medicine.

For decades a major goal of neurological research has been finding a way to prevent the formation of and to break up and destroy amyloid plaques in the brains and nervous systems of people with Alzheimer’s and other degenerative diseases before they wreak havoc.

Amyloid plaques are tightly packed sheets of proteins that infiltrate the brain. These plaques, which are stable and seemingly impenetrable, fill nerve cells or wrap around brain tissues and eventually (as in the case of Alzheimer’s) suffocate vital neurons or brain cells, causing loss of memory, language, motor function and eventually premature death.

To date, researchers have had no success in destroying plaques in the human brain and only minimal success in the laboratory. One reason for these difficulties in finding compounds that can dissolve amyloids is their immense stability and their complex composition.

Yet, Duennwald experienced success in previous studies when he exposed amyloids in living yeast cells to EGCG. Furthermore, he and his collaborators also found before that DAPH-12, too, inhibits amyloid production in yeast.

In their new study, the team decided to look in more detail at the impact of these two chemicals on the production of different amyloids produced by the yeast amyloid protein known as PSI+. They chose this yeast amyloid protein because it has been studied extensively in the past, and because it produces varieties of amyloid structures that are prototypes of those found in the damaged human brain. Thus, PSI+ amyloids are excellent experimental paradigms to study basic properties of all amyloid proteins.

The team’s first step was to expose two different amyloid structures produced by yeast (e.g., a weak version and a strong version) to EGCG. They found that the EGCG effectively dissolved the amyloids in the weaker version. To their surprise, they found that the stronger amyloids were not dissolved and that some transformed to even stronger versions after exposure to EGCG.

The team then exposed the yeast amyloid structures to a combination of the EGCG and the DAPH-12 and found that all of the amyloid structures broke apart and dissolved.

The next steps for the research team will be to explore the mechanism and potency of such a combinatorial therapy for the treatment of diverse neurodegenerative diseases.

“Our findings are certainly preliminary and we need further work to fully comprehend the effects of EGCG in combination with other chemicals on amyloids. Yet, we see our study as a very exciting initial step towards combinatorial therapies for the treatment of amyloid-based diseases,” says Duennwald.

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Authors of the study include: Martin L Duennwald and Chan Chung from Boston Biomedical Research Institute and Nicholas P Lopreiato, Elizabeth A Sweeny, M Noelle Knight, James Shorter, Huan Wang, and Blake E Roberts from the Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine.

The Boston Biomedical Research Institute is a not-for-profit institution dedicated to the understanding, treatment, and prevention of specific human diseases such as muscular dystrophy, cancer, cardiovascular disease, and Alzheimer’s. For more information, visit us on the web at www.bbri.org.

Long-term effects of statin therapy could lead to transient or permanent cognitive impairment

2009 study posted for filing

Contact: Nick Zagorski
nzagorski@asbmb.org
301-634-7366
American Society for Biochemistry and Molecular Biology

Statins show dramatic drug and cell dependent effects in the brain

Besides their tremendous value in treating high cholesterol and lowering the risk of heart disease, statins have also been reported to potentially lower the risks of other diseases, such as dementia. However, a study in the October Journal of Lipid Research finds that similar statin drugs can have profoundly different effects on brain cells –both beneficial and detrimental. These findings reinforce the idea that great care should be taken when deciding on the dosage and type of statin given to individuals, particularly the elderly.

John Albers and colleagues compared the effects of two commercially used statins, simvastatin and pravastatin, on two different types of brain cells, neurons and astrocytes (support cells that help repair damage). By directly applying the drugs to cells as opposed to administering them to animals, they could eliminate differences in the drugs’ ability to cross the blood-brain barrier as a reason for any differing effects. Albers and colleagues looked at the expression of genes related to neurodegeneration, and found that indeed, despite using biologically equivalent drug concentrations, differences were seen both between cells, and between drugs; for example, simvastatin reduced the expression of the cholesterol transporter ABCA1 by approximately 80% in astrocytes, while pravastatin lowered expression by only around 50%. Another interesting difference was that while both statins decreased expression of the Tau protein –associated with Alzheimer’s disease—in astrocytes, they increased Tau expression in neurons; pravastatin also increased the expression of another Alzheimer’s hallmark, amyloid precursor protein (APP).

While increased levels of these two proteins may account for potential risks of disease, Albers and colleagues also note that large decreases in cholesterol proteins like ABCA1 should be considered. Brain cholesterol levels tend to be reduced in elderly people, and in such individuals the long-term effects of statin therapy could lead to transient or permanent cognitive impairment.

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From the article: “Differential effects of simvastatin and pravastatin on expression of Alzheimer’s disease-related genes in human astrocytes and neuronal cells” by Weijiang Dong, Simona Vuletic and John J. Albers
Corresponding Author: John J Albers, Northwest Lipid Metabolism and Diabetes Research Laboratories, University of Washington jja@u.washington.edu

Radioprotection and extracts of Ginko biloba

Contact: Chang-Mo Kang
kangcm@kcch.re.kr
Inderscience Publishers

Herbal tonic for radiotherapy

Antioxidant extracts of the leaves of the Gingko biloba tree may protect cells from radiation damage, according to a study published in the International Journal of Low Radiation. The discovery may one day be used to help reduce side effects in cancer patients undergoing radiotherapy.

Chang-Mo Kang of the Korea Institute of Radiological and Medical Sciences in Taegu and colleagues are interested in the protective effects of well-known herbal remedies of which Gingko biloba is one. G. biloba is a unique tree species with no close living relatives and extracts of its leaves contain antioxidant compounds including glycosides and terpenoids known as ginkgolides and bilobalides.

These compounds are thought to protect cells from damage by free radicals and other reactive oxidizing species found in the body. These are generated continuously by the body’s normal metabolism, and in excess in some diseases or after exposure to pollution or radiation. They damage proteins, DNA and other biomolecules and left unchecked can kill cells.

As such, extracts of certain plants that contain antioxidants, including G. biloba, have attracted interest for their pharmacological activity. G. biloba is currently sold as a herbal supplement and there are numerous claims for health benefits, including the possibility of preventing the onset of dementia or Alzheimer’s disease.

Kang and colleagues have now collected human white blood cells, lymphocytes, from healthy donors aged 18 to 50 years. They treated half of these cells with commercially available G. biloba extract in the laboratory and doused the other half with salt solution as an experimental control. They then compared the effects of gamma radiation from radioactive cesium on the white blood cells compared to the untreated control samples.

The team uses a light microscope to look for lymphocytes undergoing programmed cell death, or apoptosis, as a result of radiation exposure. They found that there was a significant increase in apoptosis in the untreated cells compared with those treated with G. biloba extract. Almost a third of the untreated cells underwent apoptosis compared with approximately one in twenty of the treated cells. Parallel studies with laboratory mice also demonstrated a similar protective effect against radiation poisoning.

The results suggest that the extracts can neutralize the free-radicals and oxidizing agents produced in the cells by the radiation and so prevent them from undergoing apoptosis.

 

###

 

“Protective effect of Gingko biloba against radiation-induced cellular damage in human peripheral lymphocytes and murine spleen cells” in Int. J. Low Radiation, 2009, 6, 209-218

Pesticide levels in blood linked to Parkinson’s disease, UT Southwestern researchers find

2009 study posted for filing

Contact: Aline McKenzie
aline.mckenzie@utsouthwestern.edu
214-648-3404
UT Southwestern Medical Center

DALLAS – July 13, 2009 – People with Parkinson’s disease have significantly higher blood levels of a particular pesticide than healthy people or those with Alzheimer’s disease, researchers at UT Southwestern Medical Center have found.

In a study appearing in the July issue of Archives of Neurology, researchers found the pesticide beta-HCH (hexachlorocyclohexane) in 76 percent of people with Parkinson’s, compared with 40 percent of healthy controls and 30 percent of those with Alzheimer’s.

The finding might provide the basis for a beta-HCH blood test to identify individuals at risk for developing Parkinson’s disease. The results also point the way to more research on environmental causes of Parkinson’s.

“There’s been a link between pesticide use and Parkinson’s disease for a long time, but never a specific pesticide,” said Dr. Dwight German, professor of psychiatry at UT Southwestern and a senior author of the paper. “This is particularly important because the disease is not diagnosed until after significant nerve damage has occurred. A test for this risk factor might allow for early detection and protective treatment.”

About 1 million people in the U.S. have Parkinson’s, a number expected to rise as the population ages. The disease occurs when brain cells in particular regions die, causing tremors, cognitive problems and a host of other symptoms.

The study involved 113 participants, ages 50 to 89. Fifty had Parkinson’s, 43 were healthy and 20 had Alzheimer’s. The researchers tested the subjects’ blood for 15 pesticides known as organochlorines.

These pesticides, which include the well-known DDT (dichlorodiphenyltrichloroethane), were widely used in the U.S. from the 1950s to the 1970s but are more tightly regulated now. They persist in the environment for years without breaking down. In the body, they dissolve in fats and are known to attack the type of brain nerves that die in Parkinson’s disease, the researchers said.

“Much higher levels of the beta-HCH were in the air, water and food chain when the Parkinson’s patients were in their 20s and30s,” Dr. German said. “Also, the half-life of the pesticide is seven to eight years, so it stays in the body for a long time.”

Parkinson’s disease is more common among rural men than other demographic groups, but it is not a matter of a single factor causing the devastating disease, Dr. German said.

“Some people with Parkinson’s might have the disease because of exposure to environmental pesticides, but there are also genes known to play a role in the condition,” Dr. German said.

Although the current study points to an interesting link between the pesticide beta-HCH and Parkinson’s, there could be other pesticides involved with the disease, he said.

For example, the pesticide lindane often contains beta-HCH, but lindane breaks down faster. Beta-HCH might simply be a sign that someone was exposed to lindane, with lindane actually causing the damage to the brain, the researchers said.

In future research, Dr. German hopes to test patients from a wider geographical area and to measure pesticide levels in post-mortem brains. He and his team also are collecting blood samples from both patients with Parkinson’s and their spouses to see if a genetic difference might be making the one with Parkinson’s more susceptible to pesticides than the other.

###

Other UT Southwestern researchers involved in the study were Dr. Padraig O’Suilleabhain, associate professor of neurology; Dr. Ramón Diaz-Arrastía, professor of neurology; and Dr. Joan Reisch, professor of clinical sciences.

Researchers from the Robert Wood Johnson Medical School, including lead author Dr. Jason Richardson, and the Environmental and Occupational Health Sciences Institute in New Jersey also participated in the study.

The study was funded by the National Institute of Environmental Health Sciences, the National Institute on Aging, the Dallas Area Parkinsonism Society, Rowe & Co. Inc., the Dallas Foundation and the Michael J. Fox Foundation for Parkinson’s Research.

Visit www.utsouthwestern.org/neurosciences to learn more about UT Southwestern’s clinical services in neurosciences, including psychiatry.

This news release is available on our World Wide Web home page at www.utsouthwestern.edu/home/news/index.html

To automatically receive news releases from UT Southwestern via e-mail, subscribe at www.utsouthwestern.edu/receivenews

Dr. Dwight German — http://www.utsouthwestern.edu/findfac/professional/0,2356,12533,00.html

Researchers find possible environmental causes for Alzheimer’s, diabetes : nitrates

2009 study posted for filing

Contact: Nancy Cawley Jean njean@lifespan.org Lifespan

Call for reducing nitrate levels in fertilizer and water, detoxifying food and water

Providence, RI – A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food with increased deaths from diseases, including Alzheimer’s, diabetes mellitus and Parkinson’s. The study was published in the Journal of Alzheimer’s Disease (Volume 17:3 July 2009).

Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer’s, Parkinson’s, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer’s, Parkinson’s, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases.

De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, “We have become a ‘nitrosamine generation.’ In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture.” She continues, “Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking.”

Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.

Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods.

Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer’s, Parkinson’s and Type 2 diabetes mellitus.

De la Monte comments, “All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies.”

The researchers recognize that an increase in death rates is anticipated in higher age groups. Yet when the researchers compared mortality from Parkinson’s and Alzheimer’s disease among 75 to 84 year olds from 1968 to 2005, the death rates increased much more dramatically than for cerebrovascular and cardiovascular disease, which are also aging-associated. For example, in Alzheimer’s patients, the death rate increased 150-fold, from 0 deaths to more than 150 deaths per 100,000. Parkinson’s disease death rates also increased across all age groups. However, mortality rates from cerebrovascular disease in the same age group declined, even though this is a disease associated with aging as well.

De la Monte notes, “Because of the similar trending in nearly all age groups within each disease category, this indicates that these overall trends are not due to an aging population. This relatively short time interval for such dramatic increases in death rates associated with these diseases is more consistent with exposure-related causes rather than genetic changes.” She also comments, “Moreover, the strikingly higher and climbing mortality rates in older age brackets suggest that aging and/or longer durations of exposure have greater impacts on progression and severity of these diseases.”

The researchers graphed and analyzed mortality rates, and compared them with increasing age for each disease. They then studied United States population growth, annual use and consumption of nitrite-containing fertilizers, annual sales at popular fast food chains, and sales for a major meat processing company, as well as consumption of grain and consumption of watermelon and cantaloupe (the melons were used as a control since they are not typically associated with nitrate or nitrite exposure).

The findings indicate that while nitrogen-containing fertilizer consumption increased by 230 percent between 1955 and 2005, its usage doubled between 1960 and 1980, which just precedes the insulin-resistant epidemics the researchers found. They also found that sales from the fast food chain and the meat processing company increased more than 8-fold from 1970 to 2005, and grain consumption increased 5-fold.

The authors state that the time course of the increased prevalence rates of Alzheimer’s, Parkinson’s and diabetes cannot be explained on the basis of gene mutations. They instead mirror the classical trends of exposure-related disease. Because nitrosamines produce biochemical changes within cells and tissues, it is conceivable that chronic exposure to low levels of nitrites and nitrosamines through processed foods, water and fertilizers is responsible for the current epidemics of these diseases and the increasing mortality rates associated with them.

De la Monte states, “If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption.”

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Other researchers involved in the study with de la Monte include Alexander Neusner, Jennifer Chu and Margot Lawton, from the departments of pathology, neurology and medicine at Rhode Island Hospital and The Warren Alpert Medical School of Brown University.

The study was funded through grants from the National Institutes of Health. Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH and diabetes.

De la Monte, Suzanne M., Alexander Neusner, Jennifer Chu and Margot Lawton. “Epidemilogical Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer’s Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis.” Journal of Alzheimer’s Disease, 17:3 (July 2009) pp 519-529.

The Journal of Alzheimer’s Disease (http://www.j-alz.com) is an international multidisciplinary journal to facilitate progress in understanding the etiology, pathogenesis, epidemiology, genetics, behavior, treatment and psychology of Alzheimer’s disease. The journal publishes research reports, reviews, short communications, book reviews, and letters-to-the-editor. Groundbreaking research that has appeared in the journal includes novel therapeutic targets, mechanisms of disease and clinical trial outcomes. The Journal of Alzheimer’s Disease has an Impact Factor of 5.101 according to Thomson Reuters’ 2008 Journal Citation Reports. The Journal is published by IOS Press (http://www.iospress.nl).

Founded in 1863, Rhode Island Hospital (www.rhodeislandhospital.org) in Providence, RI, is a private, not-for-profit hospital and is the largest teaching hospital of the Warren Alpert Medical School of Brown University. A major trauma center for southeastern New England, the hospital is dedicated to being on the cutting edge of medicine and research. Many of its physicians are recognized as leaders in their respective fields of cancer, cardiology, diabetes, emergency medicine and trauma, neuroscience, orthopedics, pediatrics, radiation oncology and surgery. Rhode Island Hospital receives nearly $50 million each year in external research funding. It is home to Hasbro Children’s Hospital, the state’s only facility dedicated to pediatric care, which is ranked among the top 30 children’s hospitals in the country by Parents magazine. Rhode Island Hospital is a founding member of the Lifespan health system.

60th Health Research Report 07 JUL 2009 – Reconstruction

Editors Top Five:

1.Your Arteries on Wonder Bread

2.Report: Prostate cancer screening has yet to prove its worth

3. Doubts cast on credibility of some published clinical trials

4. Health food supplement may curb compulsive hair pulling

5. Acid-reducing medicines may lead to dependency

In this issue:

1.Irritability should be considered when diagnosing bipolar disorder in children

2. Kidney damage from medical imaging procedures can cause long-term health problems

3. Chemicals in common consumer products may play a role in pre-term births

4. Vitamin A derivative provides clues to better breast cancer drugs

5.Your Arteries on Wonder Bread

6. Tryptophan deficiency may underlie quinine side effects

7. Mice run faster on high-grade oil

8.Report: Prostate cancer screening has yet to prove its worth

9. Magic ingredient in breast milk protects babies’ intestines

10.K-STATE RESEARCHER STUDIES THE ANTI-CANCER CAPABILITIES OF A SPECIAL PURPLE SWEET POTATO

11.Triggering muscle development — a therapeutic cure for muscle wastage?

12.Acid-reducing medicines may lead to dependency

13.Doubts cast on credibility of some published clinical trials

14.. Caffeine reverses memory impairment in Alzheimer’s mice

15.Researchers find possible environmental causes for Alzheimer’s, diabetes

16.Muscle damage may be present in some patients taking statins

17. Health food supplement may curb compulsive hair pulling

18.Sugar substitute appears to prevent early childhood cavities

Health Research Report

60th Issue Date 07 JUL 2009

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/engineeringevil

www.engineeringevil.com

Aspirin and similar drugs may be associated with brain microbleeds in older adults: Causes amyloid accumulation often related to Alzheimer’s disease

2009 study posted for filing

Contact: Monique M.B. Breteler, M.D., Ph.D. m.breteler@erasmusmc.nl JAMA and Archives Journals

Individuals who take aspirin or other medications that prevent blood clotting by inhibiting the accumulation of platelets appear more likely to have tiny, asymptomatic areas of bleeding in the brain, according to a report posted online today that will appear in the June print issue of Archives of Neurology, one of the JAMA/Archives journals.

Cerebral microbleeds—small deposits of the iron-storing protein hemosiderin in the brain—may be a sign of cerebral small-vessel disease, according to background information in the article. This condition, common among older adults, occurs when the walls of blood vessels in the brain become weakened. When microbleeds occur in certain brain areas, they may indicate a type of small vessel disease known as cerebral amyloid angiopathy, in which the accumulation of amyloid (a protein often related to Alzheimer’s disease) causes degeneration of smooth muscle cells and increases the susceptibility of blood vessels to ruptures and hemorrhages.

Meike W. Vernooij, M.D., and colleagues at Erasmus MC University Medical Center, Rotterdam, the Netherlands, investigated the relationship between cerebral microbleeds and the use of anti-clotting medications in 1,062 individuals without dementia involved in the Rotterdam Scan Study. Participants (average age 69.6) underwent magnetic resonance imaging examinations in 2005 and 2006. Pharmacy records were used to assess whether any of the individuals took anti-clotting drugs. These included aspirin and carbasalate calcium—called platelet aggregation inhibitors because they prevent the accumulation of platelets that form blood clots.

In the years before MRI, 363 (34.2 percent) of the participants had used any anti-clotting drugs, including 245 (23.1 percent) who took platelet aggregation inhibitors (67 taking aspirin and 141 taking carbasalate calcium). Compared with patients who did not use anti-clotting drugs, those who took aspirin or carbasalate calcium were more likely to have cerebral microbleeds visible on MRI. This association was particularly strong among individuals taking these drugs at higher doses, typically used to treat or prevent heart disease. Microbleeds in the frontal lobe were more common among aspirin users than carbasalate calcium users. There was no association between other types of anti-clotting drugs and cerebral microbleeds.

“There is currently major interest in bleeding risks with the use of antithrombotic or thrombolytic treatment in persons who have microbleeds that are apparent on MRI because this may affect treatment in patients with cardiovascular or cerebrovascular disease,” the authors write. “The cross-sectional design of our analyses prohibited an investigation of whether persons with cerebral microbleeds are at increased risk for symptomatic hemorrhage [excessive bleeding] when using platelet aggregation inhibitors.”

The beneficial effects of anti-clotting drugs for individuals at risk for heart attack and stroke typically outweigh any risks of bleeding, they note. “Nevertheless, it may be that in selected persons (e.g., those with signs of cerebral amyloid angiopathy), this risk-benefit ratio may differ for certain drugs (e.g., aspirin), thus influencing treatment decision,” they conclude.

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(Arch Neurol. 2009;66[6]:(doi:10.1001/archneurol.2009.42).  Available pre-embargo to the media at www.jamamedia.org.)

Editor’s Note: Please see the article for additional information, including other authors, author contributions and affiliations, financial disclosures, funding and support, etc

Cognitive Decline Begins in Late 20s, U.Va. Study Suggests

2009 study posted for filing

 

March 18, 2009 — A new study indicates that some aspects of peoples’ cognitive skills — such as the ability to make rapid comparisons, remember unrelated information and detect relationships — peak at about the age of 22, and then begin a slow decline starting around age 27.

 

“This research suggests that some aspects of age-related cognitive decline begin in healthy, educated adults when they are in their 20s and 30s,” said Timothy Salthouse, a University of Virginia professor of psychology and the study’s lead investigator.

 

His findings appear in the current issue of the journal Neurobiology of Aging.

 

Salthouse and his team conducted the study during a seven-year period, working with 2,000 healthy participants between the ages of 18 and 60.

 

Participants were asked to solve various puzzles, remember words and details from stories, and identify patterns in an assortment of letters and symbols.

 

Many of the participants in Salthouse’s study were tested several times during the course of years, allowing researchers to detect subtle declines in cognitive ability.

 

Top performances in some of the tests were accomplished at the age of 22. A notable decline in certain measures of abstract reasoning, brain speed and in puzzle-solving became apparent at 27.

 

Salthouse found that average memory declines can be detected by about age 37. However, accumulated knowledge skills, such as improvement of vocabulary and general knowledge, actually increase at least until the age of 60.

 

“These patterns suggest that some types of mental flexibility decrease relatively early in adulthood, but that how much knowledge one has, and the effectiveness of integrating it with one’s abilities, may increase throughout all of adulthood if there are no pathological diseases,” Salthouse said.

 

However, Salthouse points out that there is a great deal of variance from person to person, and, he added, most people function at a highly effective level well into their final years, even when living a long life.

 

One of the unique features of this project in the University of Virginia Cognitive Aging Laboratory is that some of the participants return to the laboratory for repeated assessments after intervals of one to seven years.

 

“By following individuals over time, we gain insight to cognition changes, and may possibly discover ways to alleviate or slow the rate of decline,” Salthouse said. “And by better understanding the processes of cognitive impairment, we may become better at predicting the onset of dementias such as Alzheimer’s disease.”

 

Salthouse’s team also is surveying participants’ health and lifestyles to see if certain characteristics, such as social relationships, serve to moderate age-related cognitive changes.

 

They hope to continue their studies over many more years, with many of the same participants, to gain a long-term understanding of how the brain changes over time.

 

— By Fariss Samarrai

Caffeine may block inflammation linked to mild cognitive impairment

Contact: Phyllis Picklesimer p-pickle@illinois.edu 217-244-2827 University of Illinois College of Agricultural, Consumer and Environmental Sciences

URBANA – Recent studies have linked caffeine consumption to a reduced risk of Alzheimer’s disease, and a new University of Illinois study may be able to explain how this happens.

“We have discovered a novel signal that activates the brain-based inflammation associated with neurodegenerative diseases, and caffeine appears to block its activity. This discovery may eventually lead to drugs that could reverse or inhibit mild cognitive impairment,” said Gregory Freund, a professor in the U of I’s College of Medicine and a member of the U of I’s Division of Nutritional Sciences.

Freund’s team examined the effects of caffeine on memory formation in two groups of mice—one group given caffeine, the other receiving none. The two groups were then exposed to hypoxia, simulating what happens in the brain during an interruption of breathing or blood flow, and then allowed to recover.

The caffeine-treated mice recovered their ability to form a new memory 33 percent faster than the non-caffeine-treated mice. In fact, caffeine had the same anti-inflammatory effect as blocking IL-1 signaling. IL-1 is a critical player in the inflammation associated with many neurodegenerative diseases, he said.

“It’s not surprising that the insult to the brain that the mice experienced would cause learning memory to be impaired. But how does that occur?” he wondered.

The scientists noted that the hypoxic episode triggered the release of adenosine by brain cells.

“Your cells are little powerhouses, and they run on a fuel called ATP that’s made up of molecules of adenosine. When there’s damage to a cell, adenosine is released,” he said.

Just as gasoline leaking out of a tank poses a danger to everything around it, adenosine leaking out of a cell poses a danger to its environment, he noted.

The extracellular adenosine activates the enzyme caspase-1, which triggers production of the cytokine IL-1β, a critical player in inflammation, he said.

“But caffeine blocks all the activity of adenosine and inhibits caspase-1 and the inflammation that comes with it, limiting damage to the brain and protecting it from further injury,” he added.

Caffeine’s ability to block adenosine receptors has been linked to cognitive improvement in certain neurodegenerative diseases and as a protectant against Alzheimer’s disease, he said.

“We feel that our foot is in the door now, and this research may lead to a way to reverse early cognitive impairment in the brain. We already have drugs that target certain adenosine receptors. Our work now is to determine which receptor is the most important and use a specific antagonist to that receptor,” he said.

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The study appears in the Journal of Neuroscience and can be viewed online at http://www.jneurosci.org/content/32/40/13945.full. Co-authors are Gabriel Chiu, Diptaman Chatterjee, Patrick Darmody, John Walsh, Daryl Meling, and Rodney Johnson, all of the U of I. Funding for the study was provided by the National Institutes of Health.

Sleeping Brain Behaves as If It’s Remembering Something

In the background is an entorhinal cortex neuron that was studied. The blue-green trace shows neocortical slow oscillation while the yellow trace shows the persistent activity of entorhinal cortical neuron, even when the inputs from neocortex were silent. (Credit: Mayank Mehta)

ScienceDaily (Oct. 7, 2012) — UCLA researchers have for the first time measured the activity of a brain region known to be involved in learning, memory and Alzheimer’s disease during sleep. They discovered that this part of the brain behaves as if it’s remembering something, even under anesthesia, a finding that counters conventional theories about memory consolidation during sleep.

The research team simultaneously measured the activity of single neurons from multiple parts of the brain involved in memory formation. The technique allowed them to determine which brain region was activating other areas of the brain and how that activation was spreading, said study senior author Mayank R. Mehta, a professor of neurophysics in UCLA’s departments of neurology, neurobiology, physics and astronomy.

In particular, Mehta and his team looked at three connected brain regions in mice — the new brain or the neocortex, the old brain or the hippocampus, and the entorhinal cortex, an intermediate brain that connects the new and the old brains. While previous studies have suggested that the dialogue between the old and the new brain during sleep was critical for memory formation, researchers had not investigated the contribution of the entorhinal cortex to this conversation, which turned out to be a game changer, Mehta said. His team found that the entorhinal cortex showed what is called persistent activity, which is thought to mediate working memory during waking life, for example when people pay close attention to remember things temporarily, such as recalling a phone number or following directions.

“The big surprise here is that this kind of persistent activity is happening during sleep, pretty much all the time.” Mehta said. “These results are entirely novel and surprising. In fact, this working memory-like persistent activity occurred in the entorhinal cortex even under anesthesia.”

The study appears Oct. 7, 2012 in the early online edition of the journal Nature Neuroscience.

The findings are important, Mehta said, because humans spend one-third of their lives sleeping and a lack of sleep results in adverse effects on health, including learning and memory problems.

It had been shown previously that the neocortex and the hippocampus “talk” to each other during sleep, and it is believed that this conversation plays a critical role in establishing memories, or memory consolidation. However, no one was able to interpret the conversation.

“When you go to sleep, you can make the room dark and quiet and although there is no sensory input, the brain is still very active,” Mehta said. “We wanted to know why this was happening and what different parts of the brain were saying to each other.”

Mehta and his team developed an extremely sensitive monitoring system that allowed them to follow the activities of neurons from each of three targeted portions of the brain simultaneously, including the activity of a single neuron. This allowed them to decipher the precise communications, even when the neurons were seemingly quiet. They then developed a sophisticated mathematical analysis to decipher the complex conversation.

During sleep, the neocortex goes into a slow wave pattern for about 90 percent of that time. During this period, its activity slowly fluctuates between active and inactive states about once every second. Mehta and his team focused on the entorhinal cortex, which has many parts.

The outer part of the entorhinal cortex mirrored the neocortical activity. However, the inner part behaved differently. When the neocortex became inactive, the neurons in the inner entorhinal cortex persisted in the active state, as if they were remembering something the neocortex had recently “said,” a phenomenon called spontaneous persistent activity. Further, they found that when the inner part of the entorhinal cortex became spontaneously persistent, it prompted the hippocampus neurons to become very active. On the other hand, when the neocortex was active, the hippocampus became quieter. This data provided a clear interpretation of the conversation.

“During sleep the three parts of the brain are talking to each other in a very complex way,” he said. “The entorhinal neurons showed persistent activity, behaving as if they were remembering something even under anesthesia when the mice could not feel or smell or hear anything. Remarkably, this persistent activity sometimes lasted for more than a minute, a huge timescale in brain activity, which generally changes on a scale of one thousandth of a second.”

The findings challenge theories of brain communication during sleep, in which the hippocampus is expected to talk to, or drive, the neocortex. Mehta’s findings instead indicate that there is a third key actor in this complex dialogue, the entorhinal cortex, and that the neocortex is driving the entorhinal cortex, which in turn behaves as if it is remembering something. That, in turn, drives the hippocampus, while other activity patterns shut it down.

“This is a whole new way of thinking about memory consolidation theory. We found there is a new player involved in this process and it’s having an enormous impact,” Mehta said. “And what that third player is doing is being driven by the neocortex, not the hippocampus. This suggests that whatever is happening during sleep is not happening the way we thought it was. There are more players involved so the dialogue is far more complex, and the direction of the communication is the opposite of what was thought.”

Mehta theorizes that this process occurs during sleep as a way to unclutter memories and delete information that was processed during the day but is irrelevant. This results in the important memories becoming more salient and readily accessible. Notably, Alzheimer’s disease starts in the entorhinal cortex and patients have impaired sleep, so Mehta’s findings may have implications in that arena.

For this study, Mehta teamed with Thomas Hahn and Sven Berberich of Heidelberg University in Germany and the Max Planck Institute for Medical Research and James McFarland of Brown University and the UCLA Department of Physics. Going forward, the team will further study this brain activity to uncover the mechanisms behind it and determine if it influences subsequent behavioral performance.

“These results provide the first direct evidence for persistent activity in medial entorhinal cortex layer neurons in vivo, and reveal its contribution to cortico-hippocampal interactions, which could be involved in working memory and learning of long behavioral sequences during behavior, and memory consolidation during sleep,” the study states.

The study was funded by the Whitehall Foundation, the National Institutes of Health, the National Science Foundation, the W. M. Keck Foundation, the German Ministry of Education and Research and the Max Planck Society.

http://www.sciencedaily.com/releases/2012/10/121007134729.htm

45th Health Research Report 09 NOV 2008 – Reconstruction

Editors Top Five:

1. Selenium may slow march of AIDS

2. Vitamin B1 could reverse early-stage kidney disease in diabetes patients

3. Persistent pollutant may promote obesity

4. Broccoli compound targets key enzyme in late-stage cancer

5. Down’s symptoms may be treatable in the womb

In this issue:

1. Inhaled corticosteroids raise pneumonia risk for lung disease sufferers

2. Stanford/Packard study shows no benefit from drug widely used to prevent premature births

3. US infant formula safe from melamine, says FDA

4. Vitamin K linked to insulin resistance in older men

5. Down’s symptoms may be treatable in the womb

6. Selenium may slow march of AIDS

7. Fast food a potential risk factor for Alzheimer’s

8. Despite “Apology Laws,” Physicians May Not Communicate Medical Errors

9. Broccoli compound targets key enzyme in late-stage cancer

10. Persistent pollutant may promote obesity

11. Calcium and vitamin D may not be the only protection against bone loss

12. A little wine boosts omega-3 in the body: Researchers find a novel mechanism for a healthier heart

13. Flu vaccine linked to reduced illness, impairment of academic performance among college students (Read WHOLE article),,,

14. Eating eggs when pregnant affects breast cancer in offspring

15. Vitamin D found to fight placental infection

16. Interferon as long-term treatment for hepatitis C not effective, report HALT-C researchers

17. Updated standards to reduce metal contaminants in prescription drugs

18. Breaking the silence after a study ends

19. Vitamin B1 could reverse early-stage kidney disease in diabetes patients

20. Statin warning for pregnant women

21. Pine bark reduces inflammatory marker CRP in osteoarthritis

 

Health Technology Research Synopsis

45th Issue Date 09 NOV 2008

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/engineeringevil

www.engineeringevil.com

 

 

 

Vitamin B3 reduces Alzheimer’s symptoms, lesions

2008 study posted for filing

Contact: Jennifer Fitzenberger
jfitzen@uci.edu
949-824-3969
University of California – Irvine

UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients

Irvine, Calif. — An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.

Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.

“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”

The study appears online Nov. 5 in the Journal of Neuroscience.

Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.

Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.

In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.

The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.

Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.

Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.

“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”

 

###

 

LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.

The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.

For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.

UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 27,000 undergraduate and graduate students and nearly 2,000 faculty members. The third-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.6 billion. For more UCI news, visit www.today.uci.edu.

News Radio: UCI maintains on campus an ISDN line for conducting interviews with its faculty and experts. The use of this line is available free-of-charge to radio news programs/stations who wish to interview UCI faculty and experts. Use of the ISDN line is subject to availability and approval by the university.

 

UCI maintains an online directory of faculty available as experts to the media. To access, visit www.today.uci.edu/experts. For UCI breaking news, visit www.zotwire.uci.edu.

Melatonin and exercise work against Alzheimer’s in mice

Contact: SINC info@agenciasinc.es 34-914-251-820 FECYT – Spanish Foundation for Science and Technology

Different anti-aging treatments work together and add years of life

The combination of two neuroprotective therapies, voluntary physical exercise, and the daily intake of melatonin has been shown to have a synergistic effect against brain deterioration in rodents with three different mutations of Alzheimer’s disease.

A study carried out by a group of researchers from the Barcelona Biomedical Research Institute (IIBB), in collaboration with the University of Granada and the Autonomous University of Barcelona, shows the combined effect of neuroprotective therapies against Alzheimer’s in mice.

Daily voluntary exercise and daily intake of melatonin, both of which are known for the effects they have in regulating circadian rhythm, show a synergistic effect against brain deterioration in the 3xTg-AD mouse, which has three mutations of Alzheimer’s disease.

“For years we have known that the combination of different anti-aging therapies such as physical exercise, a Mediterranean diet, and not smoking adds years to one’s life,” Coral Sanfeliu, from the IIBB, explains to SINC. “Now it seems that melatonin, the sleep hormone, also has important anti-aging effects”.

The experts analysed the combined effect of sport and melatonin in 3xTg-AD mice which were experiencing an initial phase of Alzheimer’s and presented learning difficulties and changes in behaviour such as anxiety and apathy.

The mice were divided into one control group and three other groups which would undergo different treatments: exercise –unrestricted use of a running wheel–, melatonin –a dose equivalent to 10 mg per kg of body weight–, and a combination of melatonin and voluntary physical exercise. In addition, a reference group of mice were included which presented no mutations of the disease.

“After six months, the state of the mice undergoing treatment was closer to that of the mice with no mutations than to their own initial pathological state. From this we can say that the disease has significantly regressed,” Sanfeliu states.

The results, which were published in the journal Neurobiology of Aging, show a general improvement in behaviour, learning, and memory with the three treatments.

These procedures also protected the brain tissue from oxidative stress and provided good levels of protection from excesses of amyloid beta peptide and hyperphosphorylated TAU protein caused by the mutations. In the case of the mitochondria, the combined effect resulted in an increase in the analysed indicators of improved performance which were not observed independently.

Treatment not easily transferable to humans

“Transferring treatments which are effective in animals to human patients is not always consistent, given that in humans the disease develops over several years, so that when memory loss begins to surface, the brain is already very deteriorated,” the IIBB expert points out.

However, several clinical studies have found signs of physical and mental benefits in sufferers of Alzheimer’s resulting from both treatments. The authors maintain that, until an effective pharmacological treatment is found, adopting healthy living habits is essential for reducing the risk of the disease appearing, as well as reducing the severity of its effects.

The melatonin debate

The use of melatonin, a hormone synthesized from the neurotransmitter serotonin, has positive effects which can be used for treating humans. With the approval of melatonin as a medication in the European Union in 2007, clinical testing on this molecule has been increasing. It has advocates as well as detractors, and the scientific evidence has not yet been able to unite the differing views.

According to the Natural Medicines Comprehensive Database, melatonin is probably effective in sleeping disorders in children with autism and mental retardation and in blind people; and possibly effective in case of jet-lag, sunburns and preoperative anxiety.

“However, other studies which use melatonin as medication show its high level of effectiveness,” Darío Acuña-Castroviejo explains to SINC. He has been studying melatonin for several years at the Health Sciences Technology Park of the University of Granada.

The expert points out that international consensus already exists, promoted by the British Association for Psychopharmacology –also published in the Journal of Psychopharmacology in 2010–, which has melatonin as the first choice treatment for insomnia in patients above the age of 55. This consensus is now being transferred to cases of insomnia in children.

Its use in treating neurodegenerative diseases is acquiring increasing scientific support in lateral amyotrophic sclerosis, in Alzheimer’s, and Duchenne muscular dystrophy.

“Even though many more studies and clinical tests are still required to assess the doses of melatonin which will be effective for a wide range of diseases, the antioxidant and anti-inflammatory properties of melatonin mean that its use is highly recommended for diseases which feature oxidative stress and inflammation,” Acuña-Castroviejo states.

This is the case for diseases such as epilepsy, chronic fatigue, fibromyalgia, and even the aging process itself, where data is available pointing to the benefits of melatonin, though said data is not definitive.

###

Reference:

García-Mesa Y, Giménez-Llort L, López LC, Venegas C, Cristòfol R, Escames G, Acuña-Castroviejo D, Sanfeliu C. “Melatonin plus physical exercise are highly neuroprotective in the 3xTg-AD mouse”. Neurobiol Aging 2012 Jun; 33(6):1124.e13-29.

Contact:

Coral Sanfeliu Instituto de Investigaciones Biomédicas de Barcelona (IIBB) Tel.: +34 93.363.83.38 Email: coral.sanfeliu@iibb.csic.es

About melatonina:

Darío Acuña-Castroviejo Centro de Investigación Biomédica Parque Tecnológico de Ciencias de la Salud Universidad de Granada Telf.: +34 958 241000, ext. 20169 Email: dacuna@ugr.es

Oxidative stress: Mechanism of cell death clarified: ” this cell death could be completely prevented by Vitamin E, but not by water-soluble antioxidants”

2008 Posted for filing

Contact: Heinz-Jörg Haury presse@helmholtz-muenchen.de 49-893-187-2460 Helmholtz Zentrum München – German Research Center for Environmental Health

Life processes in cells require a reducing environment that needs to be sustained with the help of a large number of antioxidative enzymes. This may sound abstract and incomprehensible, but everyone knows the phenomenon that a piece of cut apple or a piece of cut meat changes colour quickly and deteriorates, because the oxygen in the air produces chemical reactions in the tissues (oxidation of biomolecules).

If the equilibrium in the organism moves towards oxidative processes, then this is known as oxidative stress. Oxidative stress, for instance, is associated with the aging of body cells. Furthermore, a strong accumulation of reactive oxygen species (ROS) along with drops in cellular concentrations of glutathione, (GSH), the major antioxidant produced by the body, is well known as a common cause of acute and chronic degenerative diseases, such as, arteriosclerosis, diabetes, stroke, Alzheimer’s and Parkinson’s diseases.

“To investigate the molecular function of the cellular reducing agent GSH in the metabolic pathway of cell death triggered by oxidative stress, mice and cells were generated that specifically lack glutathione peroxidase 4 (GPx4), which is emerging as one of the most important GSH dependent enzymes”, explains Marcus Conrad. The induced inactivation of GPx4 caused massive oxidation of lipids and eventually cell death. A similar phenotype could be observed when intracellular GSH was removed from wild-type cells by a chemical inhibitor of GSH biosynthesis.

Interestingly enough, . Since the oxidation of fatty acids in this cell death pathway, was of paramount importance, multiple studies were performed to describe, in greater detail, the source and nature of lipid peroxides.

Pharmacological and reverse genetic analyses showed that lipid peroxides in GPx4-depleted cells do not appear by coincidence, but accumulate due to increased activity of a specific enzyme of the arachidonic acid metabolism, the 12/15-lipoxygenase. Activation of apoptosis inducing factor (AIF), evidenced by its relocation from mitochondria to the cell nucleus, was identified as another important event in this signaling cascade.

The fact that oxidative stress is a major inducer of cell death is a well accepted current model. Until now however, the source and nature of the reactive oxygen species has remained obscure, as have questions concerning the way they act.  Marcus Conrad: “So far, it was assumed that oxidative stress is detrimental to cells by unspecific oxidation of many essential biomolecules, such as proteins and lipids. That is why we were amazed to find that in cells lacking either glutathione or glutathione peroxidase 4, a distinctive signaling pathway is engaged, which causes cell death. The data represent the first molecular analyses of a redox-regulated signaling pathway, describing how oxidative stress is recognized in the body and translated into cell death”.

Since this cell death cascade can be interrupted at any single stage with the help of drugs, this pathway harbors promising targets for therapeutic intervention to mitigate the deleterious effects of oxidative stress in complex degenerative human diseases.

###

Publication

Alexander Seiler, Manuela Schneider, Heidi Förster, Stephan Roth, Eva K. Wirth, Carsten Culmsee, Nikolaus Plesnila, Elisabeth Kremmer, Olof Rådmark, Wolfgang Wurst, Georg W. Bornkamm, Ulrich Schweizer, and Marcus Conrad: Glutathione Peroxidase 4 Senses and Translates Oxidative Stress into 12/15-Lipoxygenase Dependent- and AIF-Mediated Cell Death. Cell Metabolism 2008 8: 237-248.

Neural implants could spark better decisions

18:00 19 September 2012 by Douglas Heaven Magazine issue 2883.

Ever wish you could make better choices? That could one day be possible thanks to an electronic brain implant that can enhance short-term memory and decision-making in primates. The implant can also restore these functions in an animal model of Alzheimer’s disease and other types of brain damage, paving the way for the development of new treatments for people with these conditions.

Sam Deadwyler at Wake Forest University School of Medicine in Winston-Salem, North Carolina, and colleagues have previously shown that a neural implant can restore some motor and sensory functions in rats. Now they have used a similar implant to stimulate higher-level thinking in monkeys.

During normal brain function, neurons “fire” when they receive an input from another neuron via the connection between them, called a synapse. The spatial and temporal pattern of this activity  – where and when the neurons fire   – can be detected and recorded.

To find out if it is possible to hijack and then retune these patterns of activity, Deadwyler’s team first trained five rhesus macaques to perform a task that tests their attention, short-term memory and decision-making skills.

First, the monkeys were shown a random image from a pool of 5000. The image was then blanked out for an interval of 1 to 90 seconds, before reappearing in a different position, alongside up to seven other images. If the monkey selected the original image once it reappeared it was rewarded with juice.

After two years of training, the monkeys correctly matched the images 75 per cent of the time at the easier levels  – when the image was blanked out for a short period of time, and fewer images were displayed when it reappeared. Their success rate declined to 40 per cent in tasks with the longest interval and maximum amount of images to choose from.

The animals then had a device capable of recording and stimulating neuronal activity implanted into their prefrontal cortex, an area of the brain responsible for many facets of intelligence. Specifically, the implant was able to record neuronal communication in the so-called supra-granular layers (layers 2/3), part of the six layers that make up this part of the cortex, and both record from and stimulate neurons in layer 5 (see diagram). Layers 2/3 and 5 are around 1350 micrometres apart and differ in their predominant cell type and connectivity.

The challenge lay in working out which patterns of activity should be induced and when in order to enhance the monkeys’ performance in the task. To do so, the team recorded neuronal activity while the animals performed the task again. They then analysed the activity going into and out of the different layers and extracted patterns of neuronal firing that correlated with correct and incorrect decisions.

The team was then able to enhance the animals’ decision-making process by ensuring that the implant kicked in whenever the neuronal activity in layers 2/3 resembled that seen when an incorrect decision was being made. When it did, the implant stimulated a pattern of activity in layer 5 that replicated the activity recorded when a correct decision was made.

The implant was able to improve average performance in the task by 10 to 20 per cent. In the hardest versions of the task – such as when the original image reappeared alongside several other images  – the monkeys also significantly increased their speed, taking 2 rather than 3 seconds to correctly identify the image.

The team next tested the implant’s ability to restore cognitive function in monkeys that had been given cocaine. The drug is commonly used in animals to model the loss of synaptic connections seen in Alzheimer’s, dementia and other types of brain injury.

Without stimulation from the implant, the monkeys’ performance dropped by 10 per cent across all difficulty levels. When the implant was switched on, however, their performance was boosted to just below levels seen in monkeys who hadn’t been given cocaine or an implant.

“It’s a wonderful piece of work,” says Daniel Chew at the University of Cambridge, who was not involved in the study. He suggests that since the implant reduces the number of incorrect responses there may be an even greater degree of improvement on a more difficult task.

Simon Schultz at Imperial College London agrees that it is an impressive study, but says that it is not clear what exactly is going on. We understand the motor and sensory domains quite well, he says, but we still don’t know how the cortex works. These guys step around that, he says, by effectively recognising what a correct decision looks like, recording that pattern and playing it back.

In the study, the patterns of activity used to stimulate a correct answer were specific to each monkey. Would it be possible to use a pattern taken from one high-performing individual and use it to raise the game of others? According to team member Robert Hampson, giving one monkey a “correct” pattern of activity from another didn’t work, and in fact reduced performance, just as scrambled patterns did.

To apply this technology to people with conditions such as Alzheimer’s, this limitation would have to be overcome, either by learning much more about how a correct pattern is shaped from inputs into each area, or recording healthy brain activity before a person developed symptoms of brain damage.

A further problem is the invasive nature of implants. “It causes very acute inflammation and scarring,” says Chew. This can kill the neurons around the implant, insulating the electrodes and diminishing their effectiveness. Chew and his colleagues are trying to create biologically compatible electrodes to get around this problem.

Another possibility is bypassing the need for an implant entirely. Deadwyler and Hampson both point out that transcranial imaging and stimulation – the ability to visualise and stimulate activity in the brain non-invasively – is advancing quickly and that it may one day be possible to adapt their approach to work from outside the skull.

Regardless, the pair believe that human trials of the implant are in sight since similar hardware has already been approved by the US Food and Drug Administration for use in people with Parkinson’s. “[Human trials] may not be too far down the line,” says Deadwyler.

This is great news for people with brain deterioration  – the likely first participants of such a trial. But besides therapeutic treatment, the possibilities are endless. Imagine an implant in your visual cortex, says Schultz. This, he suggests, would make it possible to identify the pattern of activity that occurs when you imagine a number. When this pattern was recognised by the implant it could stimulate the pattern for a new number for you to picture. In theory, such an implant could be used to create a secure code for a cryptographic key based on values only you can access.

The problem with developing a prosthesis for cognitive enhancement rather than restoration is that it is harder to justify the trials. But, as Schultz jokes, “why stop at repair when you can enhance as well?” It’s a nice idea, but the ethical hurdles mean that developing a prosthesis for cognitive enhancement rather than restoration is not currently justifiable, he says. For the time being, at least, the focus will rightly be on ways to restore lost function in people with brain damage. And that’s surely a good decision.

Journal reference: Journal of Neural Engineering, doi.org/jcx

http://www.newscientist.com/article/dn22282-neural-implants-could-spark-better-decisions.html?full=true&print=true

Vitamin C and beta-carotene might protect against dementia

Contact: Willi Baur willi.baur@uni-ulm.de 49-731-502-2020 IOS Press

Study examines the influence of antioxidants on the pathogenesis of Alzheimer’s disease

Forgetfulness, lack of orientation, cognitive decline… about 700, 000 Germans suffer from Alzheimer’s disease (AD). Now researchers from the University of Ulm, among them the Epidemiologist Professor Gabriele Nagel and the Neurologist Professor Christine von Arnim, have discovered that the serum-concentration of the antioxidants vitamin C and beta-carotene are significantly lower in patients with mild dementia than in control persons. It might thus be possible to influence the pathogenesis of AD by a person’s diet or dietary antioxidants. 74 AD-patients and 158 healthy controls were examined for the study that has been published in the “Journal of Alzheimer’s Disease” (JAD).

AD is a neurodegenerative disease: Alterations in the brain caused by amyloid-beta-plaques, degeneration of fibrillae and a loss of synapses are held responsible for the characteristic symptoms. Oxidative stress, which constrains the exploitation of oxygen in the human body, is suspected to promote the development of AD. Whereas so called antioxidants might protect against neurodegeneration. In their study, the researchers have investigated whether the serum-levels of vitamin C, vitamin E, beta-carotene as well as lycopene and coenzyme Q10 are significantly lower in the blood of AD-patients. “In order to possibly influence the onset and development of Alzheimer’s disease, we need to be aware of potential risk factors”, says Gabriele Nagel.

Participants were recruited from the cross-sectional study IMCA ActiFE (Activity and Function in the Elderly in Ulm) for which a representative population-based sample of about 1,500 senior citizens has been examined. The 65 to 90 years old seniors from Ulm and the surrounding area underwent neuropsychological testing and answered questions regarding their lifestyle. What is more, their blood has been examined and their body mass index (BMI) was calculated. For the present study, scientists have compared 74 patients with mild dementia (average age 78.9 years) with a control group consisting of 158 healthy, gender-matched persons of the same age. Results are quite interesting: The concentration of vitamin C and beta-carotene in the serum of AD-patients was significantly lower than in the blood of control subjects. Whereas no such difference between the groups could be found for the other antioxidants (vitamin E, lycopene, coenzyme Q10). Potential confounding factors such as education, civil status, BMI, consumption of alcohol and tobacco have been considered in the statistical analysis. Nevertheless, additional parameters such as the storage and preparation of food as well as stressors in the life of participants might have influenced the findings. Therefore, results need to be confirmed in prospective surveys. “Longitudinal studies with more participants are necessary to confirm the result that vitamin C and beta-carotene might prevent the onset and development of Alzheimer’s disease”, says Gabriele Nagel. Vitamin C can for example be found in citrus fruits; beta-carotene in carrots, spinach or apricots.

###

The study has been supported by the Ministry of Science, Research and the Arts of Baden-Württemberg (as part of the Geriatric Competence Center Ulm) and by the European Union. Further authors from the University of Ulm comprise Professor Albert Ludolph (Director of the Department of Neurology) and Professor Matthias Riepe, Department of Psychiatry and Psychotherapy II, as well as Professor Richard Peter and Florian Herbolsheimer (Institute of Epidemiology and Medical Biometry). Professor Thorsten Nikolaus (Geriatric Competence Center Ulm) and Professor Hans Biesalski (University of Hohenheim) have also contributed to the study

29th Health Research Report 29 APR 2008 – Reconstruction

 

Editors Top Five:

 

1.      High blood pressure may protect against migraine
2.      Study shows pine bark naturally reduces osteoarthritis
3.      Life expectancy worsening or stagnating for large segment of the US population
4.      Study reveals inaccuracies in studies of cancer treatment
5.      Study says FDA allowed risky tests of blood substitutes

 

In this issue:

 
1.      High blood pressure may protect against migraine
2.      Excess pneumonia deaths linked to engine exhaust
3.      Vitamin E may help Alzheimer’s patients live longer
4.      Chinese club moss extract (Huperzine A) may improve cognition in Alzheimer’s disease
5.      Think twice before using antibiotics for acute maxillary sinusitis
6.      MSU study finds media coverage of breast cancer focuses too little on prevention
7.      Chemical exposure may increase risk of ALS
8.      Low vitamin D levels associated with an increased risk of peripheral arterial disease
9.      Study shows pine bark naturally reduces osteoarthritis
10.  Study reveals inaccuracies in studies of cancer treatment
11.  Life expectancy worsening or stagnating for large segment of the US population
12.  Researchers detail chemotherapy’s damage to the brain
13.  Could blood transfusions cause harm?
14.  Study shows common vitamin and other micronutrient supplements reduce risks of TB recurrence
15.  Epilepsy drug causes bone loss in young women
16.  Diabetes drugs may be related to fracture risk
17.  Osteoporosis drug may be associated with irregular heartbeat
18.  Hormone therapy in postmenopausal women associated with increased risk of stroke
19.  Aspirin-like compounds increase insulin secretion in otherwise healthy obese people
20.  Families of contaminated heparin victims tell stories of deaths 
21.  Study says FDA allowed risky tests of blood substitutes

 

Health Research Report 

29th Issue Date 29 APR 2008

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm http://www.facebook.com/vitaminandherbstore

www.engineeringevil.com

Smart drugs to ‘moral enhancement’: a chemical approach to transhumanism

By Olivia Solon 06 September 12

Steroids. Ritalin. Modafinil. Prozac. EPO. These are just a selection of drugs that could be described as boosting the cognitive or physical performance of human beings. As part of Wired.co.uk’s Transhuman Week, we take a look at what chemical enhancements there are on the horizon.
Memory enhancement

Baylor University researchers have discovered a molecule called PKR, which regulates how neurons interact in memory-related tasks. When the molecule is genetically suppressed, another immune molecule called gamma interferon steps in. The understudy molecule is much better at increasing communication between neurons and making memory more efficient. By finding a chemical inhibitor for the PKR molecule the team realised it could generate the memory boost without using genetic engineering. They found a molecule that did the trick, and it could be used to develop drugs to help Alzheimer’s patients combat memory loss. Likewise it could be used by people who don’t have Alzheimers to turbo-charge their memories.
Live strong and long

A gene called DAF-2 has been suppressed in nematode worms through genetic manipulation to allow them to live six times longer than normal. Cynthia Kenyon, who researches ageing, and her team believe the gene may also play a key role in human ageing and may be susceptible to pharmacological manipulation — Kenyon predicts within 15 years — although that should be taken with a large pinch of salt.

In the interim, we’ll just have to make do with the human growth hormone — already popular in older male Hollywood circles, HGH plays a key role in development and healing. Patients with low levels of the growth hormone might put find it hard maintaining their body weight, so can take a synthetic version of the hormone called somatropin. The drug has been shown to increase muscle strength and aerobic endurance, especially when combined with testosterone. However, joint pain and carpal tunnel syndrome came as side effects.

Combatting baldness

Male pattern baldness affects 80 percent of men at some point in their lives and no matter how convincing the claims of various cosmetic products are, there’s very little that can hold back the hair loss. However, researchers at the University of Pennsylvania have identified an enzyme called prostaglandin D2 that inhibits hair growth. Drugs that block the protein are already available on the market, being used to treat asthma and allergies, however they could be repurposed into lotions to transform wispy thinning hair into stronger, longer locks. However, it’s unclear whether it can help grow hair where “as a coot” baldness has been achieved.
Moral enhancement

Drugs that affect our perceived “moral” behaviour already exist. Anti-depressants lower aggression and can make people friendlier, and oxytocin can increase feelings of empathy (although it is a huge stretch to refer to it as the molecule that underpins human morality as neuroeconomist Paul Zak claims).

Some factions of the transhumanist community are investigating the possibility of using drugs for “moral enhancement”, or using a cocktail of drugs to change people’s emotional responses in the hope that it will somehow “improve” their moral behaviour. Clearly, we’ll need a lot more progress in understanding the incredible complexity of brain chemistry before this would be even a remote possibility. Many of the drugs in question have different effects depending on the circumstances. For example, oxytocin makes you more likely to trust members of your social group, but reduces empathy for those outside of the group.

Furthermore, it appears to presuppose an understanding of what the “right” and “wrong” emotional and behavioural response is. Despite these major challenges, it is a rich area of research, with neuroethicists exploring the possibilities of using such drugs within the criminal justice system. Could this be the late 21st century lobotomy?

http://www.wired.co.uk/news/archive/2012-09/06/chemical-enhancement

28th Health Research Report 15 APR 2008 – Reconstructed

http://healthresearchreport.me/2008/04/15/28th-health-research-report-15-apr-2008-reconstructed/

 

Editors Top Five:

 

1.      Feta cheese made from raw milk has natural anti-food-poisoning properties
2.      ‘Healing clays’ show promise for fighting deadly MRSA superbug infections, other diseases
3.      Stanford researcher criticizes FDA plans to reduce oversight of off-label drug use
4.      France may make it illegal to promote extreme thinness
5.      Inactive kids face 6-fold risk of heart disease by teen years, study finds

 

 

In This Issue:

 
1.      Could Botulinum Toxin Be Bad for You?
2.      Viruses, oxygen and our green oceans
3.      Feta cheese made from raw milk has natural anti-food-poisoning properties
4.      Stanford researcher criticizes FDA plans to reduce oversight of off-label drug use
5.      A coffee with your doughnut could protect against Alzheimer’s disease
6.      Natural trans fats have health benefits, University of Alberta study shows
7.      Essential nutrient found in eggs reduces risk of breast cancer by 24 percent
8.      Inactive kids face 6-fold risk of heart disease by teen years, study finds
9.      Clinical trial volunteers mostly indifferent — but not blind to — researchers’ financial conflicts
10.  ‘Healing clays’ show promise for fighting deadly MRSA superbug infections, other diseases
11.  Ibuprofen or acetaminophen in long-term resistance training increases muscle mass/strength
12.  Tart cherries may reduce factors associated with heart disease and diabetes
13.  Caffeine prevents multiple sclerosis-like disease in mice
14.  Ingredient Found In Green Tea Significantly Inhibits Breast Cancer Growth In Female Mice
15.  Adults who eat apples, drink apple juice have lower risk for metabolic syndrome
16.  Omega-3 intake during last months of pregnancy boosts an infant’s cognitive and motor development
17.  Getting forgetful? Then blueberries may hold the key
18.  Macadamia nuts can be included in heart healthy diet
19.  Vitamin D and calcium influence cell death in the colon, researchers find
20.  Diuretics associated with bone loss in older men
21.  Antidepressants account for only 10 percent of fall in suicide rates among older people
22.  France may make it illegal to promote extreme thinness
 

Health Technology Research Synopsis

28th Issue Date 15 APR 2008

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/vitaminandherbstore

www.engineeringevil.com

22nd Health Research Report 8 JAN 2008 – Reconstruction

Follow Link Below:

Health Technology Research Synopsis

22nd Issue Date 8 JAN 2008

Compiled By Ralph Turchiano

www.healthresearchreport.me www.vit.bz

www.youtube.com/vhfilm www.facebook.com/vitaminandherbstore

www.engineeringevil.com

Editors Top Five:

1.      The Cost of Pushing Pills: A New Estimate of Pharmaceutical Promotion Expenditures in the United States
2.      Jefferson scientists studying the effects of high-dose vitamin C on non-Hodgkin lymphoma patients
3.      100% of people carry at least one type of pesticide from the air, water or food in their bodies
4.      Treatment with NAC is associated with better outcomes for children with liver failure
5.      US ranks last among other industrialized nations on preventable deaths

 

In this issue:

 
1.      Researchers show that fibrosis can be stopped, cured and reversed
2.      Silence may lead to phantom noises misinterpreted as tinnitus
3.      The very old may benefit from L-carnitine
4.      Environmental Trigger for Alzheimer’s Disease
5.      New discovery could reduce the health risk of high-fat foods
6.      The Cost of Pushing Pills: A New Estimate of Pharmaceutical Promotion Expenditures in the United States
7.      Tips to prevent adverse drug events in older adults
8.      Vitamin D2 is as effective as vitamin D3 in maintaining concentrations of 25-hydroxyvitamin D
9.      Jefferson scientists studying the effects of high-dose vitamin C on non-Hodgkin lymphoma patients
10.  Winemaking waste proves effective against disease-causing bacteria in early studies
11.  The prevalence and impact of arthritis and other rheumatic conditions in the United States
12.  Older surgical patients at greater risk for developing cognitive problems
13.  100% of people carry at least one type of pesticide from the air, water or food in their bodies
14.  Strength training of neck muscles relieves chronic pain
15.  Treatment with NAC is associated with better outcomes for children with liver failure
16.  Pollution shrinks foetus size: Brisbane study finds
17.  Lack of vitamin D may increase heart disease risk
18.  Infants with Birthmarks Received Less Oxygen in Womb
19.  Trichloroethylene is a risk factor for parkinsonism
20.  US ranks last among other industrialized nations on preventable deaths
21.  American women are more likely to choose overly aggressive treatments for breast cancer
 
http://healthresearchreport.me/2008/01/08/22nd-health-research-report-8-jan-2008-reconstruction/

Study shows link between morbid obesity, low IQ in toddlers

Contact: April Frawley Birdwell afrawley@vpha.health.ufl.edu 352-273-5817 University of Florida

GAINESVILLE, Fla. – University of Florida researchers have discovered a link between morbid obesity in toddlers and lower IQ scores, cognitive delays and brain lesions similar to those seen in Alzheimer’s disease patients, a new study shows.

Although the cause of these cognitive impairments is still unknown, UF researchers suspect the metabolic disturbances obesity causes could be taking a toll on young brains, which are still developing and not fully protected, they write in an article published in the Journal of Pediatrics this month.

“It’s well-known that obesity is associated with a number of other medical problems, such as diabetes, hypertension and elevated cholesterol,” said Daniel J. Driscoll, M.D., Ph.D., a UF professor of pediatrics and molecular genetics and microbiology in the College of Medicine and the lead author of the study. “Now, we’re postulating that early-onset morbid obesity and these metabolic, biochemical problems can also lead to cognitive impairment.”

Researchers compared 18 children and adults with early-onset morbid obesity, which means they weighed at least 150 percent of their ideal body weight before they were 4, with 19 children and adults with Prader-Willi syndrome, and with 24 of their normal-weight siblings. Researchers chose lean siblings as a control group “because they share a socioeconomic group and genetic background,” Driscoll said.

The links between cognitive impairments and Prader-Willi syndrome, a genetic disorder that causes people to eat nonstop and become morbidly obese at a very young age if not supervised, are well-established. But researchers were surprised to find that children and adults who had become obese as toddlers for no known genetic reason fared almost as poorly on IQ and achievement tests as Prader-Willi patients. Prader-Willi patients had an average IQ of 63 and patients with early-onset morbid obesity had an average of 78. The control group of siblings had an average IQ of 106, which falls within the range of what is considered normal intelligence.

“It was surprising to find that they had an average IQ score of 78, whereas their control siblings were 106,” Driscoll said. “We feel this may be another complication of obesity that may not be reversible, so it’s very important to watch what children eat even from a very young age. It’s not just setting them up for problems later on, it could affect their learning potential now.”

While performing head MRI scans of subjects, researchers also discovered white-matter lesions on the brains of many of the Prader-Willi and early-onset morbidly obese patients. White-matter lesions are typically found on the brains of adults who have developed Alzheimer’s disease or in children with untreated phenylketonuria, the researchers wrote.

These lesions could be affecting food-seeking centers of the brain, causing the children to feel hungrier. But they are most likely a result of metabolic changes that damage the young, developing brain, Driscoll said.

More studies are needed to understand what is causing these cognitive impairments, said Merlin Butler, M.D., Ph.D., a professor of pediatrics at the University of Missouri and chief of genetics and molecular medicine at Children’s Mercy Hospital and Clinics.

“This could be a really significant observation,” Butler said. “It’s an interesting concept. It’s a whole new area of investigation.”

The findings are preliminary and additional studies are planned, Driscoll said. Jennifer Miller, M.D., a UF assistant professor of pediatric endocrinology and the first author of the study, and other researchers from UF, All Children’s Hospital in St. Petersburg, Fla., and Baylor College of Medicine also took part in the research.

Although there was no known genetic cause for early-onset morbid obesity in the subjects studied, Driscoll said there are likely genetic and hormonal factors at play that researchers have yet to discover, particularly since these children are becoming obese at a time when their parents still control what they eat. The researchers studied several sets of fraternal twins where one twin was lean and the other morbidly obese, yet their parents reported that each ate the same amount of food. In one case, the obese child actually ate less, Driscoll said.

Driscoll is also careful to point out that adults or children who become obese later in childhood are not at-risk for these cognitive impairments because their brains are sufficiently developed to fend off damage from obesity.

“We’re all mindful that this is an obese society,” he said. “We all need to be more careful with respect to what we eat, but in particular, that’s very important for children under 4.”

* Reposted for Filing

Radioprotection and extracts of Ginko biloba

Contact: Chang-Mo Kang kangcm@kcch.re.kr Inderscience Publishers

Herbal tonic for radiotherapy

Antioxidant extracts of the leaves of the Gingko biloba tree may protect cells from radiation damage, according to a study published in the International Journal of Low Radiation. The discovery may one day be used to help reduce side effects in cancer patients undergoing radiotherapy.

Chang-Mo Kang of the Korea Institute of Radiological and Medical Sciences in Taegu and colleagues are interested in the protective effects of well-known herbal remedies of which Gingko biloba is one. G. biloba is a unique tree species with no close living relatives and extracts of its leaves contain antioxidant compounds including glycosides and terpenoids known as ginkgolides and bilobalides.

These compounds are thought to protect cells from damage by free radicals and other reactive oxidizing species found in the body. These are generated continuously by the body’s normal metabolism, and in excess in some diseases or after exposure to pollution or radiation. They damage proteins, DNA and other biomolecules and left unchecked can kill cells.

As such, extracts of certain plants that contain antioxidants, including G. biloba, have attracted interest for their pharmacological activity. G. biloba is currently sold as a herbal supplement and there are numerous claims for health benefits, including the possibility of preventing the onset of dementia or Alzheimer’s disease.

Kang and colleagues have now collected human white blood cells, lymphocytes, from healthy donors aged 18 to 50 years. They treated half of these cells with commercially available G. biloba extract in the laboratory and doused the other half with salt solution as an experimental control. They then compared the effects of gamma radiation from radioactive cesium on the white blood cells compared to the untreated control samples.

The team uses a light microscope to look for lymphocytes undergoing programmed cell death, or apoptosis, as a result of radiation exposure. They found that there was a significant increase in apoptosis in the untreated cells compared with those treated with G. biloba extract. Almost a third of the untreated cells underwent apoptosis compared with approximately one in twenty of the treated cells. Parallel studies with laboratory mice also demonstrated a similar protective effect against radiation poisoning.

The results suggest that the extracts can neutralize the free-radicals and oxidizing agents produced in the cells by the radiation and so prevent them from undergoing apoptosis.

###

“Protective effect of Gingko biloba against radiation-induced cellular damage in human peripheral lymphocytes and murine spleen cells” in Int. J. Low Radiation, 2009, 6, 209-218

* Reposted for Filing

Artificial butter flavoring ingredient linked to key Alzheimer’s disease process

Public release date: 1-Aug-2012

A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer’s disease. The study appears in ACS’ journal Chemical Research in Toxicology.

Robert Vince and colleagues Swati More and Ashish Vartak explain that DA has been the focus of much research recently because it is linked to respiratory and other problems in workers at microwave popcorn and food-flavoring factories. DA gives microwave popcorn its distinctive buttery taste and aroma. DA also forms naturally in fermented beverages such as beer, and gives some chardonnay wines a buttery taste. Vince’s team realized that DA has an architecture similar to a substance that makes beta-amyloid proteins clump together in the brain — clumping being a hallmark of Alzheimer’s disease. So they tested whether DA also could clump those proteins.

DA did increase the level of beta-amyloid clumping. At real-world occupational exposure levels, DA also enhanced beta-amyloid’s toxic effects on nerve cells growing in the laboratory. Other lab experiments showed that DA easily penetrated the so-called “blood-brain barrier,” which keeps many harmful substances from entering the brain. DA also stopped a protective protein called glyoxalase I from safeguarding nerve cells. “In light of the chronic exposure of industry workers to DA, this study raises the troubling possibility of long-term neurological toxicity mediated by DA,” say the researchers.

###

The authors acknowledge funding from the Center for Drug Design (CDD) research endowment funds at the University of Minnesota, Minneapolis.

The American Chemical Society is a nonprofit organization chartered by the U.S. Congress. With more than 164,000 members, ACS is the world’s largest scientific society and a global leader in providing access to chemistry-related research through its multiple databases, peer-reviewed journals and scientific conferences. Its main offices are in Washington, D.C., and Columbus, Ohio.

To automatically receive news releases from the American Chemical Society, contact newsroom@acs.org.

Experts challenge FDA over approval for new dose of Alzheimer’s drug – Aricept ( donepezil ) Ineffective and harmful

Observations: How the FDA forgot the evidence: The case of donepezil ( Aricept) 23 mg

Approval for a new dose of a best-selling Alzheimer’s drug “breached the FDA’s own regulatory standard” and has led to “incomplete and distorted messages” about the drug, warn experts on bmj.com today.

In the first of a new occasional series, “not so”, highlighting the exaggerations, distortions, and selective reporting that mark some news stories, advertising, and medical journal articles, Lisa M. Schwartx and Steven Woloshin challenge the claims made for the new 23 mg dose of donepezil.

Professors Lisa Schwartz and Steven Woloshin of the Center for Medicine and the Media at The Dartmouth Institute for Health Policy and Clinical Practice argue that the new dose was approved “only over the objections of the FDA’s medical and statistical reviewers” and that it offers “no meaningful added benefit, just more harm.”

Donepezil was a blockbuster drug for Alzheimer’s disease, with over $2bn in annual sales in the United States alone. Just before its patent expired, the US Food and Drug Administration (FDA) approved a new 23 mg dose for moderate to severe Alzheimer’s disease, thereby extending its patent for three more years. Previously, the drug was only available in 5 mg and 10 mg doses.

The FDA and the manufacturer agreed that the 23 mg dose would be approved only if it was shown to be superior to the 10 mg dose on both a cognitive and a global functioning measure.

Although the drug improved cognitive symptoms, it did not improve overall functioning, which suggests that the cognitive difference was not meaningful. Furthermore, the new dose caused more side effects, including nausea and vomiting.

Yet Schwartz and Woloshin point to “a stunningly erroneous statement” in an advertisement aimed at doctors which claims that patients on the 23 mg dose “experienced important clinical benefit on both measures [cognition and overall functioning].”

“Nowhere – not in the direct to consumer or the physician advertisements, nor even in the FDA approved label – are the great uncertainties about this drug acknowledged, uncertainties that led the FDA’s own medical and statistical reviewers to recommend against approval of the 23 mg dose,” they argue.

Despite this, the drug was approved over the objections of the FDA’s medical and statistical reviewers and government and private insurance programmes now cover the drug. It is now, or will soon be under consideration for approval in 16 countries in Asia and South America.

Alzheimer’s is an awful disease, say the authors. “Sadly, the available drugs don’t work well. But that is no excuse for manipulating vulnerable patients, desperate family members, and their doctors to use a product that is most likely to cause net harm.”

They conclude: “To make good decisions about drugs, doctors and patients need the evidence. The FDA should not forget to give it to them.”

New material recently obtained by the authors from the FDA acknowledge that they made an error in relation to the previous label, stating: “The offending phrase was in the original label, and we don’t recall how it slipped by, but we contacted the company as soon as it was brought to our attention, and they readily agreed to remove it. We are always inter­ested in improving the content and clarity of our labeling, and appreciate being informed of any misleading or inaccurate statements that anyone may notice.”

Vitamin B3 reduces Alzheimer’s symptoms, lesions

Reposting Breakthroughs as current, to respark attention (From 2008)

UC Irvine starts clinical trial on nicotinamide effect in Alzheimer’s patients

Irvine, Calif. — An over-the-counter vitamin in high doses prevented memory loss in mice with Alzheimer’s disease, and UC Irvine scientists now are conducting a clinical trial to determine its effect in humans.

Nicotinamide, a form of vitamin B3, lowered levels of a protein called phosphorylated tau that leads to the development of tangles, one of two brain lesions associated with Alzheimer’s disease. The vitamin also strengthened scaffolding along which information travels in brain cells, helping to keep neurons alive and further preventing symptoms in mice genetically wired to develop Alzheimer’s.

“Nicotinamide has a very robust effect on neurons,” said Kim Green, UCI scientist and lead author of the study. “Nicotinamide prevents loss of cognition in mice with Alzheimer’s disease, and the beauty of it is we already are moving forward with a clinical trial.”

The study appears online Nov. 5 in the Journal of Neuroscience.

Nicotinamide is a water-soluble vitamin sold in health food stores. It generally is safe but can be toxic in very high doses. Clinical trials have shown it benefits people with diabetes complications and has anti-inflammatory properties that may help people with skin conditions.

Nicotinamide belongs to a class of compounds called HDAC inhibitors, which have been shown to protect the central nervous system in rodent models of Parkinson’s and Huntington’s diseases and amyotrophic lateral sclerosis. Clinical trials are underway to learn whether HDAC inhibitors help ALS and Huntington’s patients.

In the nicotinamide study, Green and his colleague, Frank LaFerla, added the vitamin to drinking water fed to mice. They tested the rodents’ short-term and long-term memory over time using water-maze and object-recognition tasks and found that treated Alzheimer’s mice performed at the same level as normal mice, while untreated Alzheimer’s mice experienced memory loss.

The nicotinamide, in fact, slightly enhanced cognitive abilities in normal mice. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said LaFerla, UCI neurobiology and behavior professor.

Scientists also found that the nicotinamide-treated animals had dramatically lower levels of the tau protein that leads to the Alzheimer’s tangle lesion. The vitamin did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion.

Nicotinamide, they found, led to an increase in proteins that strengthen microtubules, the scaffolding within brain cells along which information travels. When this scaffolding breaks down, the brain cells can die. Neuronal death leads to dementia experienced by Alzheimer’s patients.

“Microtubules are like highways inside cells. What we’re doing with nicotinamide is making a wider, more stable highway,” Green said. “In Alzheimer’s disease, this highway breaks down. We are preventing that from happening.”

###

LaFerla and Green are affiliated with the Institute for Brain Aging and Dementia, which is conducting the clinical trial with funding from the Alzheimer’s Association.

The institute seeks volunteers who have been diagnosed with Alzheimer’s, are 50 or older, and have a friend or relative who can accompany them to clinic visits and answer questions. Study participants will take the vitamin supplement or a placebo twice daily for 24 weeks, with seven visits to the UCI clinic.

For more information on the clinical trial, contact Beatriz Yanez at 949-824-5733.

UCI scientists Joan Steffan, Hilda Martinez-Coria, Xuemin Sun, Steven Schreiber and Leslie Thompson also worked on the study, which was supported in part by the Alzheimer’s Drug Discovery Foundation and the National Institutes of Health.

About the University of California, Irvine: The University of California, Irvine is a top-ranked university dedicated to research, scholarship and community service. Founded in 1965, UCI is among the fastest-growing University of California campuses, with more than 27,000 undergraduate and graduate students and nearly 2,000 faculty members. The third-largest employer in dynamic Orange County, UCI contributes an annual economic impact of $3.6 billion. For more UCI news, visit www.today.uci.edu.

News Radio: UCI maintains on campus an ISDN line for conducting interviews with its faculty and experts. The use of this line is available free-of-charge to radio news programs/stations who wish to interview UCI faculty and experts. Use of the ISDN line is subject to availability and approval by the university.

UCI maintains an online directory of faculty available as experts to the media. To access, visit www.today.uci.edu/experts.  For UCI breaking news, visit www.zotwire.uci.edu.

Deer antlers inspire a new theory on osteoporosis

The loss of manganese could mean that calcium does not stick to bones and could cause osteoporosis. This is the new theory put forward by researchers at the University of Castilla-La Mancha (UCLM) in Spain after studying deer antlers. The hypothesis published this month in the Frontiers of Bioscience journal still needs to be confirmed by the scientific community.

Through the study of deer antlers, researchers of the Research Institute of Hunting Resources (IREC, joint centre UCLM-CSIC-JCCM) suggest that the origin of osteoporosis could not be directly linked to the lack of calcium but rather to the lack of a mineral essential to calcium absorption. In particular they believe that this could be manganese, according to a new theory published in the latest issue of the Frontiers of Bioscience journal.

According to Tomás Landete, sub-director of the IREC and one of team’s researchers, “previous antler studies show that manganese is necessary for calcium absorption. Our hypothesis is that when the human body absorbs less manganese or when it is sent from the skeleton to other organs that require it, such as the brain, the calcium that is extracted at the same time is then not properly absorbed and is excreted in the urine. It is in this way that osteoporosis can slowly strike.”

The theory must now be validated with more studies and medical trials but its creators believe that it is a “step in a totally new direction in osteoporosis research as it considers calcium loss to be a consequence of the disease and not the origin.”

The idea for the new proposal came from a dramatic increase in antler breakages seen in Spain in 2005. When scientists analysed these antlers in detail, they realised that weakening was due to manganese depletion caused by the deer’s diet. That year saw an intensely cold winter which in turn caused plants to reduce their manganese concentrations in response to such stress.

“Antlers grow by transferring 20% of the skeleton’s calcium towards their structure. We therefore saw that it was not calcium deficiency that caused the weakening but rather the deficiency of manganese,” clarifies Landete. “The lack of manganese was almost as if the ‘glue’ that sticks calcium to antlers bones was missing.”

Links to Alzheimer’s and Parkinson’s Disease

In the case of humans, the researchers suggest that manganese is extracted from the bones when it is required by the “most important” organs, such as the brain. The researcher adds that “maintaining the bones is important, but even more so is sustaining the working of the brain, which uses 25% of our energy intake when at rest.”

The team also points out that when this vital mineral runs out after the onset of osteoporosis, conditions like Alzheimer’s disease, Parkinson’s disease, and senile dementia could strike. To put this theory to the test, they analysed data from 113 patients who were operated on for osteoporosis and osteoarthritis (wear and tear of joint cartilage) at Hellín Hospital in Albacete, Spain between 2008 and 2009. Some 40% of those operated on for osteoporosis showed some form of cerebral dysfunction whereas this was not the case in any of the 68 patients operated on for osteoarthritis.

Furthermore, the percentage increased with age and only amongst those patients with osteoporosis. The exhaustion of manganese reserves could be behind the bone disease and the cerebral degeneration. “We are collecting human bones to confirm this. However, studies on rats in which Alzheimer’s disease has been induced by aluminium intoxication show that as the severity of this disease increases, manganese levels in the bones decrease,” says Landete.

The researcher also recalls studies that link manganese to Parkinson’s disease and show that astrocytes, which provide support to neurons, have specific enzymes that require manganese. In any case, researchers outline that their theory “is not a final solution to such diseases but constitutes the first step in a new direction” – a new direction that requires validation and confirmation from the scientific community.

###

References:

Tomas Landete-Castillejos, Inmaculada Molina-Quilez, Jose Antonio Estevez, Francisco Ceacero, Andrés José García, Laureano Gallego. “Alternative hypothesis for the origin of osteoporosis: The role of Mn”. Frontiers in Bioscience (Elite Edition) 4: 1385-1390, January 2012. Doi: 10.2741/468

A Common Microbe Could Help To Trigger Alzheimers

 

A COMMON microbe could help to trigger Alzheimer’s disease, say researchers in the US. If true, their controversial claim could turn the multimillion-dollar field of Alzheimer’s research on its head and force a rethink on how to prevent the disease.

The microbe in question is Chlamydia pneumoniae, which is spread by coughs and sneezes. By the age of 20, half the population have been infected with C. pneumoniae, and the likelihood of being infected increases with age. The bacterium has already been accused of triggering atherosclerosis-blocked arteries that can lead to heart attacks (“Can you catch a heart attack?”, New Scientist, 8 June 1996, p 38).

Alan Hudson at Wayne State University in Detroit and his colleagues did postmortems on the brains of 19 Alzheimer’s patients and 19 people of the same age who had died of other causes. They found signs of C. pneumoniae in 17 of the Alzheimer’s sufferers, in the hippocampus and temporal cortex. These are the parts of the brain which usually sustain most damage in Alzheimer’s disease. Unaffected areas of the brain were much less likely to harbour the bacterium. The bacterium turned up in the brain of only one of the non-Alzheimer’s patients.

The team also managed to culture the microbe from two of the affected brains, showing that the organism was still alive rather than a long-dead bystander (Medical Microbiology and Immunology, vol 187, p 23).

C. pneumoniae’s presence in the diseased brains does not mean that it cause Alzheimer’s, the scientists stress. But they think the bacterium may at least be a risk factor. Chlamydia bacteria do cause inflammation when they attack other parts of the body. And the brains of people with Alzheimer’s are inflamed and contain high levels of messenger chemicals called cytokines, which trigger inflammation.

Hudson says the bacterium infects microglia and astroglia, the cerebral cousins of scavenger cells called macrophages, and this produces inflammatory cytokines. “It seems reasonably likely that C. pneumoniae could be causing the inflammation,” says Hudson.

Author: Phyllida Brown New Scientist issue 15th August 1998, page 24

PLEASE MENTION NEW SCIENTIST AS THE SOURCE OF THIS ARTICLE